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PubMed1997

[Relation between levels of essential fatty acids in maternal milk, in maternal blood and in the blood of neonates 1 and 5 days after birth].

BACKGROUND: Linolenic, linoleic, and arachidonic acids as well as other polyunsaturated fatty acids are necessary for health as the precursors of eicosanoids and for the structure of developing membranes. OBJECTIVES: The aim of the present study was the determination of the level of 11 individual free fatty acids (FFA) in the milk and in the blood of mothers and newborns during the perinatal period. METHODS: In 21 women the FFA was determined in their colostrum as well as in the venous blood at the delivery in the hospital, and then again 5 days later at leaving the hospital. Simultaneously, the blood of newborns was collected as umbilical samples at birth and as venous blood on the 5th day. The study was performed on health term infants and mothers with normal gestational age. RESULTS: The results show a marked increase in total milk FFA as well as in most, but not all, individual FFAs during the followed period of the first 5 days. The values in the milk were always remarkably higher (the increase more than 2 orders) than in the blood. We have found no significant statistical correlation between values in the blood and those in the milk. The concentrations of all very important omega-3 FFAs (which are present in fish oil and in foods of marine fish origin) were always lower in all blood and milk samples in comparison with the levels of omega-6 FFAs (which are prevailing in lipids of our usual nutrition as are margarines and most of commercial oils). CONCLUSIONS: Our findings seem to be very important for preventive medicine and need to study further the relationship of low intake of O3FA to increased incidence of various allergies and other pathological syndromes in children. The very large range of a variance in the values of FFAs in the milk suggests the need of more profound study of the role of the food composition probably during the whole period of pregnancy, mainly as to the type of lipid composition. (Tab. 1, Fig. 6, Ref. 24.)

Fatty Acids, Nonesterified↗

PubMed2002

[Analysis of maternal mortality in the Czech Republic in 2000].

OBJECTIVE: Analysis of maternal mortality in the Czech Republic in 2000. DESIGN: Retrospective statistical and clinical analysis. SETTING: Department of Obstetrics and Gynecology of the 1st Medical School of Charles University and General University Hospital, Prague 2, Institute for the Care of Mother and Child, Prague. INTRODUCTION: We present an annual analysis of maternal mortality in the Czech Republic, organized into two parts: 1) international statistical part, and 2) clinical part in Czech only with abbreviated anonymous analysis of individual cases of maternal death. We are aware that follow-up analysis cannot fully express dramatic situations around all cases or reproduce in details all their aspects. We though believe that this form will help to our gynecologists to learn about courses of the deaths, particularly when the frequency of such cases is low and circumstances are unusual. Individual analyses include also conclusions of expert committees or analyses performed by the Czech Medical Chamber. Comments and notes however are not for forensic purposes and are used only for medical ones. METHODS: We used a database of 10 cases of maternal deaths in the Czech Republic in 2000. We analyzed their causes, clinical courses, especially in connection to obstetrical surgery, and adequacy of provided care. RESULTS: There were 10 reported maternal deaths in connection to pregnancy, labor and delivery or within 42 days after delivery in the Czech Republic in 2000. There were 90,910 live-born babies and total, gross maternal mortality (A + B + C) was 0.11 per 1000, i.e. 11 deaths per 100,000 live-born babies. This is only 0.02 per 1000 better than results in 1999 (Table 3 shows data on maternal mortality for last 10 years). In 2000, there was one maternal death unrelated to gestation--category C, therefore maternal mortality in connection to gestation (A + B) was 0.099 per 1000 i.e. 9.9 deaths per 100,000 live-born babies compared to 10.1 deaths in 1999. The causes of deaths were different. Only two women were within group A (specific risk--direct maternal mortality), therefore direct maternal mortality was 2.2 per 100,000 live-born babies. Seven maternal deaths were in the group B (non-specific risk--indirect maternal mortality) and indirect maternal mortality was unusually high, 7.7 per 100,000 live-born babies. It is difficult to judge the difference due to possible error of small numbers. The demographic part of the report has been sent to the Office of Health Statistics and Information and detailed report to the Department of Health Care of the Ministry of Health of the Czech Republic. CONCLUSIONS: Since 1994, when we introduced nationwide organization measures to identify risk groups of pregnant women and use of micro-heparinization among those, we have succeeded to lower the frequency of thrombolism, till then leading cause of maternal deaths, especially in links to operative deliveries and in smaller extent among high-risk women during pregnancy. The decrease of maternal mortality was substantial, by 50%, however only temporary, followed by a partial increase to about 10 maternal deaths per 100,000 live-born babies. This increase was to increased frequency of coagulopathies, HELLP syndrome, and, in 2000, due to non-specific cardiovascular causes and some neurologic complications. The majority of these cases and especially those with non-adequate obstetrical care will be anonymously analyzed together with responsible chiefs of ob/gyn departments during perinatology conference in 2002 and results will be consequently published. Increase of non-specific causes of maternal deaths in 2000, especially of those with cardiovascular complications, indicate a necessity to be careful especially with older parturients, diabetic women, obese women and "dangerous" multiparae, where the possibility of cardiovascular complications might require need concentrated medical diagnosis. Primary attention, though, should be aimed at impaired coagulation of blood. The cases of complications of DIC persistently show insufficient diagnostic and therapeutic measures especially in small facilities with limited laboratory compartments, outdated and wrong therapeutic measures and almost missing potential for consultancy. In spite of this it is particularly necessary to concentrate on prevention among cases with higher risk for DIC. We have concentrated on publications in collaboration with hematologists and anesthesiologists in this field, although some measures are lacking the universal consent, especially some therapeutic means. It is very important to us that chiefs of ob/gyn departments are open for professional discussions, although some situations are prone to forensic evaluation. We believe that our approach of anonymous analyses with two-year delay is sufficient for necessary audit of maternal mortality.

Adult↗

PubMed1997

Maternal, placental and cord zinc components in healthy women with different levels of serum zinc.

Serum zinc is known to decrease during pregnancy, but the range of individual values at the end of normal gestation may be considerably large, with uncertain physiological significance in terms of maternal zinc status and maternal-fetal transfer of zinc. In this study we compared several maternal and cord blood indices of zinc status, placental zinc, placental metallothionein and the relationship between maternal, cord and placental components, in 40 healthy pregnant women at delivery with different levels of serum zinc. Subjects were divided into three groups according to serum zinc using as cutoff points the lower and upper quartile values [LZn, < 7.6 mumol/l (n = 10); MZn, 7.6-10.7 mumol/l (n = 20), and HZn, > 10.7 mumol/l (n = 10)]. Habitual zinc intakes were similar in all groups (average 11.5 mg/day). Considering all women, maternal serum and erythrocyte zinc correlated significantly (r = 0.40; p = 0.021). Maternal erythrocyte zinc was higher (p < 0.01) in HZn compared to the other groups. Maternal and cord values of serum zinc correlated significantly (r = 0.43; p = 0.006). Cord serum zinc values were very similar in LZn and MZn but were higher (p < 0.01) in HZn. Cord erythrocyte zinc levels were similar in all groups and about 20-25% of the maternal values. Cord erythrocyte metallothionein levels were also similar in all groups and similar to maternal values. Comparing the percentage distribution of zinc in maternal and cord serum fractions, major differences were observed in HZn, with zinc in albumin fraction being 70% in cord compared to 56% in maternal serum. There was a higher (p < 0.01) percentage of zinc bound to alpha 2-macroglobulin fraction in maternal serum of HZn compared to maternal serum of the other groups. Maternal and cord zinc in the albumin fractions correlated significantly (r = 0.48; p = 0.002) particularly in HZn (r = 0.71; p < 0.021). Placental zinc correlated negatively (r = -0.34; p = 0.035) with zinc in the maternal alpha 2-macroglobulin fraction, but did not relate to placental metallothionein, which had similar levels in all groups (average 0.28 nmol/g wet tissue). Placental zinc levels were lower (p < 0.01) in HZn. Our results indicate that high levels of maternal serum zinc in healthy women at delivery may be related to maternal tissue zinc redistribution that could favor diffusional components of maternal-fetal transfer of zinc.

Body Mass Index↗

PubMed1990

Evaluation of elevations in maternal serum alpha-fetoprotein: a review.

Maternal serum AFP screening has had significant clinical impact on reducing unrecognized anencephaly and open neural tube defects at delivery. In addition, a growing number of other associations with maternal serum AFP elevations have become apparent since antepartum screening has become commonplace. We present in this review a clinically oriented approach to understanding the physiologic basis of maternal serum AFP elevations, both true- and false-positives. Compartmentalization of etiology, fetal and maternal, and routes of communication, amniotic fluid and placenta, allows a more logical approach to developing a differential diagnosis in this group of patients. In evaluating an elevation in maternal serum AFP, it is first necessary to consider the amount of fetal production by confirming the gestational age of the fetus and the number of fetuses present. Adjustments for maternal factors (weight, race, diabetes) must also be made. Fetal developmental defects which may lead primarily to leakage of the fetal proteins into the surrounding amniotic fluid with secondary elevations of maternal serum AFP enter into the differential diagnosis. The placenta itself is probably not a production source of AFP, but when the placenta is abnormal, a greater amount of AFP may be transported to the maternal circulation. Although our thoughts frequently do turn first to an increased maternal serum AFP reflecting an increased AFP concentration in the amniotic cavity with greater transference "across the membranes," in fact a far more common etiology is an increased transfer from the fetal circulation to the maternal via the fetal-maternal interface within the placenta. This is supported by the simple fact that the vast majority of maternal serum AFP elevations are not associated with amniotic fluid AFP elevations; the amniotic fluid AFP concentrations are usually normal. Thus, in circumstances where the fetal anatomy is grossly normal and there is not another explanation for elevations in maternal serum AFP, the placenta, either secondary to providing increased areas of transport or in providing an abnormal endothelial barrier, allows for greater transfer of fetal serum, and thus AFP, into the maternal compartment. An abnormal placenta is also a likely explanation for the increased risk of adverse pregnancy outcome that is associated with increased maternal serum AFP elevations for which no obvious etiology is found. The case herein reported suggests that an abnormal placenta which provides an altered interface for AFP flow between the fetal and maternal circulations may in fact be the etiology of the significant elevations of maternal serum AFP seen in cases of triploidy.(ABSTRACT TRUNCATED AT 400 WORDS)

Abnormalities, Multiple↗

PubMed1987

Clinical high-risk designation does not predict excess fetal-maternal hemorrhage.

During a 5-year period, an enzyme-linked antiglobulin test was used to screen and quantitate fetal-maternal hemorrhage in 789 consecutive D-negative mothers who were delivered of D-positive babies. Six hundred seventy-two patients (85.2%) had no detectable fetal-maternal hemorrhage, and 117 patients (14.8%) had a detectable fetal-maternal hemorrhage. Eight of the 789 (1%) had a fetal-maternal hemorrhage greater than 30 ml and required more than one vial of Rh immune globulin. Two patients with fetal-maternal hemorrhage of 29 and 30 ml also received additional Rh immune globulin. Each case was reviewed for the presence of high-risk features that are thought to predict patients at risk for fetal-maternal hemorrhage. Patients having a cesarean section or complicated vaginal delivery were considered to be in a group at high risk for fetal-maternal hemorrhage, while those with a spontaneous vaginal delivery were considered not to be at risk for fetal-maternal hemorrhage. Thirty-two of 237 patients (13.5%) in the risk group and 82 of 552 patients (15.3%) in the group not at risk had detectable fetal-maternal hemorrhage. The incidence of fetal-maternal hemorrhage for these two groups was not statistically different (p greater than 0.50 by chi 2 analysis). If only patients in the risk group had been screened for fetal-maternal hemorrhage, then five of 10 (50%) who required more than one vial of Rh immune globulin would have been undertreated and at risk for developing anti-D antibodies. In addition, newborn birth weight, Apgar scores, and hematocrits were examined for 13 cases of fetal-maternal hemorrhage of greater than or equal to 21 ml, and none of these characteristics could be used to predict patients at risk for fetal-maternal hemorrhage. Therefore, no maternal or newborn characteristics could be identified that would reliably predict patients at risk for fetal-maternal hemorrhage. We conclude that all D-negative patients with D-positive babies should continue to be screened for fetal-maternal hemorrhage to identify those patients requiring more than one vial of Rh immune globulin.

Delivery, Obstetric↗

PubMedDate not supplied

Maternal age as a factor in determining the reproductive and behavioral outcome of rats prenatally exposed to ethanol.

Nulliparous Long-Evans rats were bred at one of four different ages and assigned to one of three treatment groups within each age condition. Maternal ages were 9, 18, 32, and 36 weeks. Treatment groups were ethanol (E), administered by gavage as 8 g/kg in two divided doses on days 10-14 of gestation, pair-fed (PF) controls, administered as an isocaloric sucrose solution by gavage on days 10-14 of gestation, and ad lib fed controls (C). All offspring were surrogate fostered shortly after delivery to untreated recently parturient dams. Litter sizes were standardized to 8 on the day of birth. Offspring were assessed longitudinally for growth, mortality, and behavior (olfaction, locomotor activity, maze learning, avoidance acquisition and startle). Approximately 85% of the 36 week old dams did not produce viable litters. In the remaining maternal age conditions, ethanol delayed offspring olfactory orientation and increased locomotor activity, the latter dissipating after 50-60 days of age. These ethanol-related effects occurred independent of maternal age condition. Maternal age, independent of ethanol, was a factor which reduced litter size and offspring weight up to 50 days, but produced few effects on behavior. The combination of maternal age and prenatal ethanol interacted to increase pregnancy loss (oldest maternal age), reduce offspring weight up to day 99 (oldest and middle maternal age), alter olfactory orientation performance (oldest and middle maternal age), reverse the typical ethanol-induced increase in activity for males in the figure-8 test (oldest maternal age group), shift the pattern of open-field activity, and change errors in a complex water maze. Not all of these interactions turned out to be specific to the ethanol X old maternal age condition. Several of the interactions occurred in both the old and middle maternal age conditions. The only effect of old maternal age that interacted strongly with ethanol was in their combined effects on reproduction. Here the combination of the two factors increased maternal mortality, the number of early pregnancy losses, and the number of litters where all members were dead or resorbed. It was concluded that short-term prenatal ethanol combined with advanced maternal age produces additive interactions on pregnancy success without affecting longer-term outcomes, while young maternal age showed no clear detrimental effects compared to the middle maternal age reference group.

Aging↗

PubMed2000

Maternal mortality, United States and Canada, 1982-1997.

BACKGROUND: The 1998 public awareness campaign on Safe Motherhood called attention to the issue of maternal mortality worldwide. This paper focuses upon maternal mortality trends in the United States and Canada, and examines differentials in maternal mortality in the United States by maternal characteristics. METHODS: Data from the vital statistics systems of the United States and Canada were used in the analysis. Both systems identify maternal deaths using the definition of the World Health Organization's International Classification of Diseases. Numbers of deaths, maternal mortality rates, and confidence intervals for the rates are shown in the paper. RESULTS: Maternal mortality declined for much of the century in both countries, but the rates have not changed substantially between 1982 and 1997. In this period the maternal mortality levels were lower in Canada than in the United States. Maternal mortality rates vary by maternal characteristics, especially maternal age and race. CONCLUSIONS: Maternal mortality continues to be an issue in developed countries, such as the United States and Canada. Maternal mortality rates have been stable recently, despite evidence that many maternal deaths continue to be preventable. Additional investment is needed to realize further improvements in maternal mortality.

Adult↗

PubMed2001

Altered placental structure induced by maternal food restriction in guinea pigs: a role for circulating IGF-II and IGFBP-2 in the mother?

Maternal feed restriction may restrict fetal growth in part indirectly by impairing placental functional development. Such actions could be mediated by the insulin-like growth factors (IGF), which are important modulators of placental growth and differentiation and more generally, are influenced by nutrient availability. While a role for the fetal IGF axis has been demonstrated, less is known of the influence, if any, of that in the mother. This study aimed to determine whether alterations in the maternal IGF axis and placental functional and structural development due to maternal food restriction are related. We therefore examined the associations between placental structural parameters, the ratios of maternal to fetal plasma glucose and fetal to maternal plasma urea concentration, and maternal circulating IGF-I, IGF-II and IGFBP-2 in ad libitum fed and food restricted (70-90 per cent of the ad libitum intake) pregnant guinea pigs. In mid-gestation, fetal weight (r = 0.65, P = 0.008, n = 17), volume of the maternal blood space (r = 0.58, P = 0.048, n = 17), and surface density of syncytiotrophoblast (r = 0.65, P = 0.023, n = 17), were positively correlated, and syncytiotrophoblast thickness was negatively correlated, with maternal plasma IGF-II concentration (r = -0.69, P = 0.014, n = 17). Late in gestation, fetal weight, placental weight and total exchange surface area in the placenta were each negatively correlated with maternal plasma IGFBP-2 concentration (all P < 0.01), while the arithmetic mean thickness of syncytiotrophoblast was positively correlated with maternal plasma IGFBP-2 concentration. Late in gestation, the ratio of maternal to fetal plasma glucose was positively correlated with fetal weight (r = 0.54, P = 0.038, n = 15) and the ratio of fetal to maternal plasma urea concentration was positively correlated with placental weight (r = 0.52, P=0.046, n=15). Maternal feed restriction reduced the ratio of maternal plasma IGF-II to IGFBP-2 in late gestation by 75 per cent (P = 0.001) and this ratio was positively correlated with fetal weight (r = 0.56, P = 0.01, n = 20), placental weight (r = 0.59, P = 0.006), placental diameter (r = 0.621, P = 0.003), placental volume (r = 0.57, P=0.009), weight of trophoblast (r = 0.51, P=0.037), weight of fetal capillaries (r = 0.49, P = 0.046), syncytiotrophoblast surface density (r = 0.611, P = 0.009) and negatively correlated with syncytiotrophoblast thickness (r = -0.55, P = 0.021). Our results suggest that in mid-pregnancy, maternal circulating IGF-II promotes placental structural development, while later in pregnancy, IGFBP-2 inhibits it, and their relative abundance and interaction strongly influences placental structure and function near term.

Animals↗

PubMedDate not supplied

Recognition of maternal identity in preterm and fullterm mothers.

The purpose of this exploratory and descriptive study was to investigate the maternal role attainment process of the preterm mother by comparing the endpoint of the process--maternal identity--in preterm and fullterm mothers. Forty-two first-time mothers, 21 preterm mothers and 21 fullterm mothers, were interviewed once at approximately one year post-birth. Qualitative and quantitative phenomena were examined. Qualitative data were collected via semi-structured interviews. Quantitative data were collected with instruments that measured maternal role attainment variables. Content analysis of the maternal identity recognition event revealed eight commonly discussed themes. Analysis of the quantitative data revealed no statistically significant relationships between length of gestation and any of the maternal role attainment variables. Also, no difference was found between preterm and fullterm mothers in the mean timing of the recognition of maternal identity. However, a 10-week difference in the median timing of maternal identity recognition was found. Sixty-two percent of the fullterm mothers recognized a maternal identity by two weeks after delivery, whereas only 24% of the preterm mothers experienced maternal identity recognition within this time frame. A statistically significant relationship was found between the timing of maternal identity recognition and maternal affective perception of the infant. The more positive the maternal affective perception of the infant, the earlier was the timing of maternal identity recognition. The study concluded that preterm mothers experienced a maternal role attainment process similar to fullterm mothers except that identity recognition was relatively delayed. The themes described by the preterm mothers tended to be qualitatively different and focused on denied maternal role experiences, especially denied contact with the infants and denied rights in relation to the infants.

Adult↗

PubMedDate not supplied

Maternal influences on cord blood lead levels.

We constructed models of umbilical cord blood lead (PbB), with and without the addition of maternal PbB at delivery and earlier in pregnancy, to determine which factors explaining cord PbB depended upon maternal PbB and which did not. We prospectively studied women of low-to-middle socioeconomic status who lived in the Valley of Mexico from 12 weeks of pregnancy to delivery. We measured maternal venous PbB during pregnancy and at delivery, and umbilical cord PbB (1-38 micrograms/dl, 0.05-1.83 mumol/l). We used multiple regression analyses to model cord PbB and a logit analysis to model the maternal-cord PbB relationship. Older mothers using lead-glazed pottery and canned foods delivered babies with increased cord PbB, while those with occasional alcohol use during pregnancy, high milk intake, and more spontaneous abortions delivered babies with lower cord PbB. Maternal PbB at 36 weeks of pregnancy and at delivery independently explained additional variance in cord PbB, but maternal PbB earlier in pregnancy did not. Some of the effects of lead-glazed pottery, maternal abortions, alcohol use, and canned food use on cord PbB were mediated through maternal PbB. The effects of maternal age and milk intake on cord PbB were independent of their influence on maternal PbB near delivery. Cord PbBs were higher than maternal PbBs at delivery in 33% of the cases, and were predominant in mothers over 30 and those drinking milk less than once per day. Measurable influence of maternal PbB on delivery cord PbB is limited to the four to eight weeks prior to delivery. Many factors suspected of influencing bone lead also control cord PbB, some of them independently of their effect on maternal delivery PbB. Minimizing fetal exposure near the end of pregnancy may require long-term control of maternal lead exposure and good management of pregnancy and diet.

Adolescent↗

PubMed1999

Localization of micro- and intermediate filaments in non-pregnant uterus and placenta of the mink suggests involvement of maternal endothelial cells and periendothelial cells in blood flow regulation.

Maternal stem arteries and arterioles of the endotheliochorial mink placenta have been shown to lack smooth muscle cells, suggesting a muscle-free attenuation of the maternal arterial pulse wave of the placenta. Since the endotheliochorial type of placenta by definition does not contain any maternal supportive tissue (e.g. connective tissue), except for the specialized interstitial layer, the aim of this study was to reveal cytoskeletal components able to compensate for the lack of conventional regulatory mechanisms of maternal placental blood flow. The study was undertaken on buffered formalin fixed tissues from 19 minks by immunohistochemistry and transmission electron microscopy to localize three major cytoskeletal filaments (desmin, vimentin and alpha-smooth muscle actin (alpha-sm-actin)) in non-pregnant uteri and placenta. The contractile alpha-sm-actin was immunodetected in the maternal subepithelial and periglandular connective tissue cells of the cyclic endometrium and during early gestation. During the transition from early- to mid gestation, maternal periendothelial cells appeared and showed alpha-sm-actin immuno-positivity; however, in late gestation, this activity could not be detected because the periendothelial cells had disappeared. Fetal endothelial cells displayed intense alpha-sm-actin immunoreactivity, which was in contrast to the alpha-sm-actin negative maternal endothelial cells. Allantochorionic mesenchymal cells also exhibited intense alpha-sm-actin immunostaining. Vimentin was immunohistochemically expressed in endothelial cells (maternal as well as fetal), maternal periendothelial cells, allantochorionic mesenchymal cells, and maternal connective tissue cells from early gestation. Desmin was not immunohistochemically detectable in cyclic endometrium and placental tissues. Transmission electron microscopy revealed the periendothelial cells to be enclosed by a thin interstitial layer. Additionally, the maternal endothelial cells displayed actin myofilament-like structures anchored basally. From our data we conclude that maternal periendothelial cells, immunoreactive for contractile actin, and maternal endothelial cells, possessing actin myofilament-like ultrastructures, act as supportive systems in the maternal vessel walls, probably influencing the regulation of the maternal blood flow.

Animals↗

PubMed1996

Direct and maternal genetic covariances by age of dam for weaning weight.

Weaning weights of calves of dams at ages in years of 2, 3, and older were modeled to be three separate traits. Fixed effects were sex of calf-year of birth combinations for nine pure breeds and sex of calf-year of birth-generation for three composite populations. Random effects fitted for each trait were correlated direct and maternal genetic, maternal permanent environmental, and temporary environmental. Direct and maternal effects were correlated across traits. A multiple-trait, derivative-free REML algorithm was used to estimate the 30 (co)variance components. Number of animals per breed group ranged from 1,244 to 4,326. For the three traits for pure breeds, average proportions of phenotypic variance were .34, .31, and .27 for direct genetic; .16, .15, and .12 for maternal genetic; and .18, .20, and .17 for maternal environmental effects. Average correlations among the three traits were .84 for direct genetic, .78 for maternal genetic, and .71 for maternal environmental effects. Average of direct-maternal genetic correlations for pure breeds was .05. For the composite breeds, average proportions of phenotypic variances were .44, .46, and .36 for direct genetic; .06, .06, and .05 for maternal genetic; and .16, .14, and .14 for maternal environmental effects. Average correlations among the three traits were .93 for direct genetic, .76 for maternal genetic, and .85 for maternal environmental effects. Average direct-maternal genetic correlation was .09 for composites. No evidence was found for greater direct-maternal genetic correlation for earlier than for later ages of dam. Sign and magnitudes of direct-maternal genetic correlations seemed to differ among pure breeds and were reflected in composites from those parent breeds.

Aging↗

PubMed2005

Permanent alterations in stress responsivity in female offspring subjected to combined maternal lead exposure and/or stress.

Elevated lead (Pb) exposures preferentially impact low socioeconomic status (SES) populations, the same groups thought to sustain the highest levels of environmental stress. As co-occurring risk factors, therefore, Pb and stress could interact, a possibility further supported by the fact that both act on mesocorticolimbic dopamine systems of the brain. We recently demonstrated in rats that maternal Pb exposure could permanently increase basal corticosterone levels of offspring consistent with altered hypothalamic pituitary adrenal (HPA) axis function. The current study was thus designed to test the hypothesis that stress responsivity of offspring should likewise be altered, with the outcome differing in response to Pb, stress or Pb+stress. The impact of intermittent variable stress challenges (restraint, novelty, cold) on behavior sensitive to Pb exposure (fixed interval (FI) schedule-controlled responding) and on stress-induced corticosterone changes were evaluated in adult female offspring of dams that had been exposed to Pb (150 ppm) in drinking water from 2 months prior to breeding through lactation with or without maternal restraint stress on days 16 and 17 of gestation. This design yielded four treatment groups: (NS/0, no maternal Pb, no maternal stress; S/0, no maternal Pb, maternal stress; NS/150, maternal Pb, no maternal stress; and S/150, maternal Pb exposure and maternal stress). While maternal Pb alone and stress alone each altered components of stress responsivity, the greatest number of effects was seen in response to Pb + stress. This included alterations in FI performance following both restraint and cold stress and in the corticosterone response to cold stress. Collectively, these studies reveal that maternal Pb exposure alone can permanently alter stress responsivity and that the profile of effects produced by maternal Pb differ from those produced by maternal Pb in conjunction with stress, findings which have both mechanistic and risk assessment significance.

Animals↗

PubMed2006

Developmental plasticity of HPA and fear responses in rats: a critical review of the maternal mediation hypothesis.

Developmental plasticity of HPA and fear responses in rats has been proposed to be mediated by environment-dependent variation in active maternal care. Here, we review this maternal mediation hypothesis based on the postnatal manipulation literature and on our own recent research in rats. We show that developmental plasticity of HPA and fear responses in rats cannot be explained by a linear single-factor model based on environment-dependent variation in active maternal care. However, by adding environmental stress as a second factor to the model, we were able to explain the variation in HPA and fear responses induced by postnatal manipulations. In this two-factor model, active maternal care and environmental stress (as induced, e.g., by long maternal separations or maternal food restriction) exert independent, yet opposing, effects on HPA reactivity and fearfulness in the offspring. This accounts well for the finding that completely safe and stable, as well as, highly stressful maternal environments result in high HPA reactivity and fearfulness compared to moderately challenging maternal environments. Furthermore, it suggests that the downregulation of the HPA system in response to stressful maternal environments could reflect adaptive developmental plasticity based on the increasing costs of high stress reactivity with increasingly stressful conditions. By contrast, high levels of environmental stress induced by environmental adversity might constrain such adaptive plasticity, resulting in non-adaptive or even pathological outcomes. Alternatively, however, developmental plasticity of HPA and fear responses in rats might be a function of maternal HPA activation (e.g., levels of circulating maternal glucocorticoid hormones). Thus, implying a U-shaped relationship between maternal HPA activation and HPA reactivity and fearfulness in the offspring, increasing maternal HPA activation with increasing environmental adversity would explain the effects of postnatal manipulations equally well. This raises the possibility that variation in active maternal care is an epiphenomenon, rather than a causal factor in developmental plasticity of HPA and fear responses in rats. Developmental plasticity of HPA and fear responses in rats and other animals has important implications for the design of animal experiments and for the well-being of experimental animals, both of which depend on the exact underlying mechanism(s). Importantly, however, more naturalistic approaches are needed to elucidate the adaptive significance of environment-dependent variation of HPA reactivity and fearfulness in view of discriminating between effects reflecting adaptive plasticity, phenotypic mismatch and pathological outcomes, respectively.

Animals↗

PubMed2002

Epidemiological evidence that maternal diabetes does not appear to increase the risk for Down syndrome.

In 1997, Narchi and Kulaylat, studying the incidence of Down syndrome in infants of gestational diabetic mothers, concluded that maternal diabetes increases the risk for Down syndrome, but failed to control the maternal age in their analysis. Using data from the Spanish Collaborative Study of Congenital Malformations (ECEMC), we analyzed the relationship between Down syndrome and maternal diabetes mellitus, and maternal gestational diabetes, controlling the maternal age through the pair-matching analysis, stratifying by maternal age and logistic regression analysis. The analyses show that maternal age is related either to Down syndrome as well as to both types of maternal diabetes. Thus, the overall analysis could be confounded by maternal age. Once we controlled the maternal age, the risk of maternal diabetes mellitus for Down syndrome is: odds ratio (OR) = 0.92 (0.41-2.07); P = 0.83. Controlling maternal age in gestational diabetes, the risk is OR = 1.18 (0.61-2.35); P > 0.70. Based on our results, we conclude that Down syndrome is related to maternal age, but does not seem to be related to any type of maternal diabetes.

Adult↗

PubMed1992

Effects of transections to the vomeronasal nerves or to the main olfactory bulbs on the initiation and long-term retention of maternal behavior in primiparous rats.

While the onset of maternal behavior at parturition is mediated by hormones, the maintenance of maternal behavior during the first few postpartum weeks depends on experiences acquired while the dam interacts with pups (Rosenblatt, 1990). In fact, if female rats are permitted as little as 2 h or maternal experience within 36 h after Cesarean delivery, they exhibit heightened maternal behavior during maternal induction tests 10 days later; in contrast, dams separated from young at the time of Cesarean delivery and not permitted a maternal experience fail to respond maternally in tests 10 days later (Orpen & Fleming, 1987). In this study we investigated the role of chemosensory input through the vomeronasal and main olfactory systems in this maternal experience effect. Six groups of primiparous females were tested for maternal behavior to foster pups presented 9-10 days after Cesarean delivery: three groups were permitted to interact with pups for a 2-h period 36 h after Cesarean delivery; and three groups were separated from pups until testing and were given no maternal experience. Within each experience condition, one group sustained bilateral section of the vomeronasal nerves, one sustained bilateral coronal cuts through the midsection of the main olfactory bulbs, and one group sustained small medial olfactory bulb cuts. The results showed that animals sustaining vomeronasal or olfactory transections, regardless of experience condition, exhibited significantly reduced latencies to maternal behavior in maternal induction tests. However, these chemosensory disruptions did not prevent an additional facilitation of maternal behavior produced by a prior maternal experience.

Animals↗

PubMed2003

Maternal antibody blocks humoral but not T cell responses to BVDV.

Bovine viral diarrhoea virus (BVDV) contributes significantly to health-related economic losses in the beef and dairy industry. Antibodies of maternal origin can be protective against BVDV infection, however, calves with low titres of maternal antibody or that do not receive colostrum may be at risk for acute BVDV infection. Interference by high titres of maternal antibodies prevents the development of an antibody response following vaccination with either a killed or attenuated BVDV vaccine. However, the T cell mediated immune response to BVDV may be generated in the absence of a detectable serum neutralizing antibody response. Two trials were conducted to evaluate the potential to elicit T cell mediated immune responses to BVDV in calves with circulating maternal antibody to BVDV. In the first trial, calves with high levels of circulating maternal antibody to BVDV 1 and BVDV 2 were experimentally infected with BVDV 2 (strain 1373) at two to five weeks of age. The T-cell mediated immune responses of the experimentally infected calves and non-infected calves were monitored monthly until circulating maternal antibody was no longer detectable in either treatment group. Calves experimentally infected with BVDV developed BVDV specific CD4(+), CD8(+), and delta T cell responses while high levels of maternal antibody were circulating. A second challenge with BVDV 2 (strain 1373) was performed in the experimentally infected and control calves once maternal antibody could no longer be detected. Previous exposure to BVDV in the presence of maternal antibody protected calves from clinical signs of acute BVDV infection compared to the control calves. In the second trial, three groups of calves with circulating maternal antibody to BVDV were given either a modified live vaccine (MLV) containing BVDV 1 and BVDV 2, a killed vaccine containing BVDV 1 and BVDV 2, or no vaccine, at seven weeks of age. Serum neutralizing antibody levels and antigen specific T cell responses were monitored for 14 weeks following vaccination. Calves vaccinated with MLV BVDV developed BVDV 1 and BVDV 2 specific CD4(+)T cell responses, and BVDV 2 specific gammadelta T cell responses, in the presence of maternal antibody. Vaccination with killed BVDV did not result in the generation of measurable antigen specific T cell immune responses. In this trial, a second vaccination was performed at 14 weeks to determine whether an anamnestic antibody response could be generated when calves were vaccinated in the presence of maternal antibody. Calves vaccinated with either a MLV or killed BVDV vaccine while they had maternal antibody developed an anamnestic antibody response to BVDV 2 upon subsequent vaccination. The results of these trials indicate that vaccinating young calves against BVD while maternal antibody is present may generate BVDV specific memory T and B cells. The data also demonstrated that seronegative calves with memory T and B cells specific for BVDV may be immune to challenge with virulent BVDV.

Animals↗

PubMed2006

Maternal microchimerism in healthy adults in lymphocytes, monocyte/macrophages and NK cells.

During pregnancy some maternal cells reach the fetal circulation. Microchimerism (Mc) refers to low levels of genetically disparate cells or DNA. Maternal Mc has recently been found in the peripheral blood of healthy adults. We asked whether healthy women have maternal Mc in T and B lymphocytes, monocyte/macrophages and NK cells and, if so, at what levels. Cellular subsets were isolated after fluorescence activated cell sorting. A panel of HLA-specific real-time quantitative PCR assays was employed targeting maternal-specific HLA sequences. Maternal Mc was expressed as the genome equivalent (gEq) number of microchimeric cells per 100,000 proband cells. Thirty-one healthy adult women probands were studied. Overall 39% (12/31) of probands had maternal Mc in at least one cellular subset. Maternal Mc was found in T lymphocytes in 25% (7/28) and B lymphocytes in 14% (3/21) of probands. Maternal Mc levels ranged from 0.9 to 25.6 and 0.9 to 25.3 gEq/100,000 in T and B lymphocytes, respectively. Monocyte/macrophages had maternal Mc in 16% (4/25) and NK cells in 28% (5/18) of probands with levels from 0.3 to 36 and 1.8 to 3.2 gEq/100,000, respectively. When compared to fetal Mc, as assessed by quantification of male DNA in women with sons, maternal Mc was substantially less prevalent in all cellular subsets; fetal Mc prevalence in T and B lymphocytes, monocyte/macrophages and NK cells was 58, 75, 50 and 62% (P=0.01, P=0.005, P=0.04, P=0.05) respectively. In summary, maternal Mc was identified among lymphoid and myeloid compartments of peripheral blood in healthy adult women. Maternal Mc was less frequent than fetal Mc in all cellular subsets tested. Studies are needed to investigate the immunological effects and function of maternal Mc and to explore whether maternal Mc in cellular subsets has biological effects on her progeny.

Adolescent↗