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Results for “Maternal Age--statistics”

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At least 19 recordsLinked to original sources
PubMed2001

Power spectrum analysis of heart rate and blood flow velocity variability measured in the umbilical and uterine arteries in early pregnancy: a comparative study.

OBJECTIVE: To compare power spectral derived variability parameters from the fetal side of the placental circulation with those from the maternal side of the placental circulation, during early pregnancy. METHODS: Doppler velocity waveforms were obtained from both the umbilical and the uterine arteries in a study group of 40 pregnant women between 10 and 14 (n = 25) and 15 and 20 (n = 15) weeks of gestation. The coefficient of variation of both the beat-to-beat heart rate variability and the blood flow velocity variability was determined. The ratio of the integrated low-frequency components (< 0.2 Hz) and the integrated high-frequency components (> 0.2 Hz) from normalized power spectrum analysis (LH-ratio) was established, to reflect sympathovagal balance. RESULTS: The coefficient of variation and LH-ratio of fetal heart rate variability constitute only a fraction of the same maternal heart rate variability parameters. Nevertheless a highly significant increase (P < 0.001) in LH-ratio was demonstrated with advancing gestational age. The coefficient of variation and LH-ratio of blood flow velocity variability were significantly lower in the fetal umbilical artery only in the 10-14-weeks' gestation group. Due to a decrease of the maternal uterine blood flow velocity variability parameters with advancing gestational age, statistically equal fetal and maternal values for coefficient of variation and LH-ratio were found in the 15-20 weeks' gestation group. CONCLUSIONS: The increase in LH-ratio of fetal heart rate variability indicates functional development of the fetal autonomic nervous system at 15-20 weeks' gestation. The umbilical blood flow velocity variability may be secondary to maternal uterine arterial flow variability rather than due to primary changes in fetal cardiovascular function.

Blood Flow Velocity↗
PubMed1996

The relation between serum markers in the second trimester and placental pathology. A study on extremely small for gestational age fetuses.

OBJECTIVES: To examine whether in women who are delivered of an extremely small for gestational age infant, raised levels of second trimester maternal serum alpha-fetoprotein (MSAFP) or human chorionic gonadotrophin (MShCG) levels are related to the presence of placental pathology detected at birth. DESIGN: Retrospective cross-sectional study. SETTING: Department of Obstetrics and Gynaecology, Antenatal Diagnosis Unit, Groningen University Hospital, The Netherlands. PARTICIPANTS: Eighty-four women who were delivered of an extremely SGA infant (< 2.3rd centile) in whom the MSAFP and the MShCG levels were known and placental pathology reports were available (study group), and 8692 women in whom the MSAFP and MShCG levels were known and the pregnancy outcome was normal (control group). Pregnancies with congenital anomalies were excluded. Analyte levels were expressed in multiples of the median (MoM) for gestational age. Statistical analysis between groups was performed by ANOVA, after logarithmic transformation of the MoMs, to normalise their distribution. MAIN OUTCOME MEASURES: 1. The means of the MSAFP and MShCG concentrations in the study group with and without placental lesions were compared with those in the control population. 2. The means of the MSAFP and MShCG levels in the study group with placental lesions were compared with those in the study group without placental lesions. RESULTS: 1. Comparison of study groups with controls: in the study group without placental lesions, the mean log MSAFP MoM (0.062), as well as the mean log MShCG MoM (-0.033), was not significantly different (P = 0.11 and P = 0.68, respectively) from the mean analyte levels in the control population (0.002 and 0.006, respectively). The mean logs of these analytes in the study group with placental lesions (0.162 and 0.129, respectively) were significantly higher compared with the MSAFP and MShCG levels in the control population (P < 0.001 for both analytes). 2. Comparison of study groups with each other: the mean log of the MSAFP level of 0.162 in the group with placental lesions was significantly different from the mean of 0.062 of the study group without placental lesions (P < 0.025). The higher mean log MShCG MoM of 0.129 in the group with placental lesions was significantly different from the mean log MShCG MoM of -0.033 in the study group without placental lesions (P < 0.025). CONCLUSIONS: Raised levels of second trimester MSAFP and MShCG in women who are subsequently delivered of an extremely small for gestational age infant are related to the presence of pathological changes in the placenta, detectable at birth. It is speculated that these placental pathological changes, which frequently accompany small for gestational age pregnancies, have their origin in the second trimester, when the normal physiological changes of the placenta occur.

Analysis of Variance↗
PubMed1999

MR imaging of hypervascular liver tumors: timing optimization during the arterial phase.

To analyze the optimal timing strategy for the detection of hypervascular liver tumors during the arterial phase of magnetic resonance (MR) imaging, a test examination after injection of 2 mL of gadopentetate dimeglumine was performed in 47 patients. The time course of the tumor-to-liver contrast-to-noise ratio (CNR) for all studies together was determined relative to the start of injection, the time of peak aortic enhancement, and the time of peak enhancement in the tumor. All studies were grouped together and the highest CNR was transiently observed at the time of peak tumor enhancement. This CNR was significantly higher than those observed at fixed delays after peak aortic enhancement. However, the CNRs at peak tumor enhancement+/-1.5 seconds did not differ significantly from those obtained after peak aortic enhancement. Finally, the CNRs obtained at fixed delays after the start of injection remained significantly lower. In hypervascular liver tumors, a higher CNR can be obtained during the arterial phase when the MR imaging delay is determined relative to the time of peak enhancement in the tumor or the aorta rather than being fixed after the start of contrast material injection. Timing based on the enhancement profile in the tumor rather than in the aorta should be performed only if rapid MR imaging is available with a time resolution of about 1.5 seconds to image the whole liver.

Adenoma↗
PubMed1984

The pathophysiology of neurofibromatosis: IX. Paternal age as a factor in the origin of new mutations.

Von Recklinghausen neurofibromatosis is characterized by a relatively large proportion of apparently nonfamilial cases, presumed spontaneous mutations. This paper analyzes the distribution of paternal and maternal ages for 187 patients with von Recklinghausen disease representing the first definite case in their respective families. Mean paternal age was 32.8 years and mean maternal age was 27.4 years, both being significantly greater than for control populations (P equal to or less than .001). The advanced paternal age was not accounted for by the increase in maternal age. The methodology of controlling the general population paternal ages for each patient's birth year is described.

Adult↗
PubMed1977

Statistical methods for detecting a moderate paternal age effect on incidence of disorder when a maternal one is present.

A statistical method is developed for detecting a moderate effect on the incidence of a disorder caused by advancing age of one parent when it is known that advancing age of the other parent is of great aetiological importance. The method is a conditional test procedure given the parental ages, therefore no assumptions about the parental age distributions have to be made. The method is applied on Danish material on Down's syndrome, for which a paternal age effect is demonstrated. Methods used in some well-known previous investigations have been discussed. Several of them, e.g. the classical one of Penrose (1933), could hardly detect any paternal age effect in Down's syndrome on the available data, because these methods are heavily affected by certain fertility patterns not recognized previously.

Denmark↗
PubMed1978

On data and methods in investigations on parental-age effects. Comments on a paper by J. D. Erickson.

An analysis of the NIS data used by Erickson (1977) has revealed that this data contains too few Down's syndrome cases with older fathers. Thus the data is less suited for an investigation of a possible paternal age effect. In addition, the statistical tests used by Erickson have low power, so that they are unable to detect a moderate paternal-age effect. Our analysis has demonstrated that discussions on paternal-age effects and similar problems should be based on high-quality data. The investigation is better based on a small high-quality material than on a large one with serious underascertainment. In the latter case one has to be extremely careful because the missing observations nearly always have common characteristics which may cause serious bias of relevant kinds.

Adult↗
PubMed1978

Down syndrome, paternal age, maternal age and birth order.

Recent cytogenetic evidence has shown that trisomy 21 can arise, perphaps even in substantial proportion, from paternal nondisjunction. The statistical association between Down syndrome incidence and maternal age, paternal age and birth order has been studied in a sample of over 4000 cases. The size of this sample made it possible to control for the effect of maternal age by single years of age during the search for a paternal age effect and vice versa, and the importance of such stringent control is emphasized. The maternal age association was confirmed with an extremely high degree of statistical significance while no independent effect of paternal age was found; indeed, the rates at paternal ages over 45 years appear to be nearly constant. After adjusting for the effects of parental age, a significant inverse association of birth order with incidence was noted. It also appears that the incidence among very young mothers may be high: for maternal ages 15 years and less the rates seem to be equivalent to those found at 30 or 35 years. In order to help answer the question of whether the maternal age association is the result of increasing rates of nondisjunction or of some other mechanism (for example, an age related defect in a spontaneous abortion screening mechanism), the proportion of cases due to maternal and paternal nondisjunction at different parental ages must be determined.

Adolescent↗
PubMed1981

Down syndrome associated with father's age in Norway.

Records of births in Norway in 1967 to 1978 were examined for evidence of an increased risk of Down syndrome associated with older paternal age. From among some 685 000 total births with known maternal and paternal age, 693 cases of Down syndrome were reported to the Medical Birth Registry of Norway. The effect of paternal age was assessed by classifying fathers as young and old on the basis of several definitions. The effect of maternal age was removed by stratifying the data on single years of mothers' age. When fathers were considered young if they were less than or equal to 49 and old if they were less than or equal to 50, the analysis yielded a statistic for the test of a one-sided hypothesis which was significant at the 0.05 level. There appears to be an increase risk (perhaps 20 to 30%) of Down syndrome associated with older fathers, independent of maternal age effect. If this increase does in fact exist, it is much smaller than the increases in risk associated with advancing maternal age, and because older men contribute a relatively small proportion of total births their contribution to the communal burden of Down syndrome is quite small. However, the finding is of aetiological interest and is the first indication of a significant paternal age effect where control for maternal age has been stringent.

Down Syndrome↗
PubMed1982

Parental age and birth order in Chinese children with congenital heart disease.

Parental age and birth order were studied in 100 Chinese children with congenital heart disease (proven by cardiac catheterisation) and in 100 controls. A higher incidence of congenital heart disease was present in the children with higher birth orders. No relationship was found between the incidence and the paternal or maternal ages. Using the method of multiple regression analysis this birth order effect was significant (p less than 0.01) and independent of parental age. This finding provides indirect evidence of environmental influence in the causation of congenital heart disease, which is known to be inherited in a multifactorial manner. Family planning to limit the size of the family may possibly contribute to the reduction of the incidence of congenital heart disease.

Adult↗
PubMed1987

Spontaneous mutation and parental age in humans.

A statistical analysis of parental age and the incidence of new mutation has been performed. Some new data on Apert, Crouzon, and Pfeiffer syndromes is presented and combined with all available data from the literature on parental age and new mutation. Significant heterogeneity among syndromes for the rate of increase in incidence with parental age was found. A parsimonious conclusion is that mutations fall into two groups, one with a high rate of increase with age and the other with a low rate of increase with age. For the high-rate-of-increase group, a linear model relating incidence to age is rejected, while an exponential model is not. In addition, for this group, increased paternal age cannot account for the observed increase in maternal age--that is, increased maternal age also contributes to the incidence of new mutations. For the low-rate-of-increase group, increased paternal age alone can account for the observed increase in maternal ages; also, either a linear or exponential model is acceptable. In addition, there is no evidence for a mixture of parental age-independent cases with parental age-dependent cases for any of the syndromes examined. The curves reflecting incidence of new mutation and paternal age for two syndromes, Apert and neurofibromatosis, have an anomalous shape. In both cases the curve increases up to age 37 and drops at age 42 before increasing again at age 47. The usual explanation for the effect of parental age on new mutations is the mechanism of "copy-error" at mitotic division in male sperone that specifies an increased probability of mutation with time spent by a spermatozoon or ovum in a haploid state, a period of time that may also increase with age of the parent. A firm answer to the question of parental age and new mutation awaits identification of the molecular defect underlying some of these syndromes; we will then be in a position to determine in which parent the mutation occurred and at what age it did so.

Acrocephalosyndactylia↗