A test for seasonality of events with a variable population at risk.
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A statistical significance test to detect seasonality of epidemiological events is described. The method is similar to that of Edwards, but makes it possible to allow for an arbitrary pattern of variation in the population risk, and also for the unequal lengths of time sectors of a cycyle of seasons (e.g., months of a year). From the test it is possible to estimate the amplitude of seasonal variation and the time at which the maximum occurs in a postulated simple harmonic fluctuation; the adequacy of the description of the data by a curve of this kind may be evaluated using a goodness-of-fit test. A numerical example of the calculations is given using some anencephalus data, and the results are compared with those of alternative tests. (+info)
Seasonal variation in anencephalus in Canada.
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A study of the monthly numbers of stillbirths and of deaths due to anencephalus in Canada from 1954 to 1962 showed a weak tendency to a winter excess of affected births. The seasonal trend was more marked in the Prarie provinces and in Quebec than elsewhere; the maximum rate of anencephalus occurrence was in October to December in the Prairies and in British Columbia, and in January to March in other regions. (+info)
The ontogenesis of human fetal hormones. III. Prolactin.
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The synthesis and release of human prolactin (hPRL) in the human fetus was assessed by radioimmunoassay analysis of the content and concentration of hPRL in 82 pituitary glands and the concentration of serum hPRL in 47 fetuses of gestational age 68 days to term. Fetal hPRL exhibited parallelism with the reference standard (Lewis 203-1). hPRL was detected by 68 days of gestation (10 wk), the earliest fetal pituitary gland studied; 8 out of 33 pituitaries had a prolactin (PRL) content above 2.0 ng between 10-15 wk gestation. The mean ocntent of PRL in the pituitary gland increased sharply from 14.8 plus or minus 4.6 ng at 15-19 wk to 405 plus or minus 142 ng at 20-24 wk and 542 plus or minus ng at 25-29 wk gestation. By term, the mean content was 2,039 plus or minus 459 (range 493-3,689) and the mean concentration 15.9 plus or minus 2.4 ng/mg (range 7-20). There was a significant positive correlation (P less than 0.001) between the hPRL and human growth hormone (hGH) content of fetal pituitary glands; at term the hPRL/hGH ratio was 1/290. The concentration of serum hPRL between 12 and 24 wk ranged from 2.9 to 67 ng/ml, mean 19.5 plus or minus 2.5 ng/ml )n = 21); by 26 wk fetal serum hPRL increased sharply and attained levels of 300-500 ng/ml in late gestation. At delivery, the mean plasma concentration of hPRL was 167 plus or minus 14.2 ng/ml in 36 umbilical venous specimens and 111.8 plus or minus 12.3 ng/ml in the matched maternal venous specimens. No correlation between serum hPRL and the pituitary content or concentration of hPRL was demonstrable in 12 matched fetal specimens. In five anencephalic infants, umbilical venous hPRL levels were between 65 and 283 ng/ml. In two anencephalic infants, thyrotropin releasing factor (TRF) (200 mug IV) evoked a rise in serum hPRL in one patient from 43 to 156 ng/ml at 30 min, and in the other from 65 to 404 ng/ml at 120 min. In both patients, plasma thyroid-stimulating hormone (TSH) rose from undetectable base-line levels to peak levels of 97 and 380 muU/ml, respectively. The pattern of change in serum hPRL in the human fetus contrasts sharply with that of serum hGH, luteinizing hormone, or follicle-stimulating hormone. These observations in the fetus and in anencephalic infants suggest that the striking elevation of serum PRL in the fetus is neither mediated by a putative PRL releasing factor or by TRF, nor is a consequence of suppression or absence of PRL release inhibiting factor alone, as a functional hypothalamus is not required to attain the high PRL concentration at term. Several lines of evidence support the view that high plasma estrogen levels characteristic of gestation act directly on the fetal anterior hypophysis to stimulate PRL secretion or to sensitize the secretory mechanism of the lactotrope, increasing its responsiveness to other stimuli. (+info)
Folic acid and prevention of spina bifida and anencephaly. 10 years after the U.S. Public Health Service recommendation.
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In September 1992, the U.S. Public Health Service (USPHS) recommended that all women capable of becoming pregnant should consume 400 microg of folic acid/day on an ongoing basis to reduce their risk for having a pregnancy affected by spina bifida and anencephaly (i.e., neural tube defects [NTDs]). The recommendation was preceded a year earlier by a CDC recommendation for women at high risk (i.e., those women who have had an earlier pregnancy affected by an NTD). The 1991 CDC recommendation stated that women at high risk should plan subsequent pregnancies and consume 4,000 microg/day of folic acid from the time they begin trying to become pregnant through the first trimester of pregnancy to reduce their risk. The 1992 USPHS recommendation specified that women at high risk should follow the general population recommendation for consumption of 400 microg/day when not trying to become pregnant. (+info)
Spina bifida and anencephaly prevalence--United States, 1991-2001.
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Spina bifida and anencephaly are serious birth defects. To reduce the occurrence of these birth defects, the Food and Drug Administration authorized the fortification of all enriched cereal grain products with folic acid in March 1996, with compliance mandatory by January 1998. This report reviews data reported to CDC's National Center for Health Statistics (NCHS) regarding spina bifida and anencephaly prevalence for live births in the United States during 1991-2001. Since 1989, NCHS has compiled birth defect data from checkboxes that appear on birth certificates. For consistency in trends, this report uses data for 1991-2001 from all U.S. reporting areas except Maryland, New Mexico, and New York. Data for 2001 are preliminary. During 1996-2001, a 23% decline occurred in neural tube defects (spina bifida and anencephaly combined). Spina bifida declined 24% during this period, and anencephaly declined 21%. The United States has experienced declines in spina bifida and anencephaly cases since folic acid fortification of all enriched cereal grain products. The observed declines have translated into approximately 920 infants being born without these serious defects each year. Continued monitoring of the occurrence of spina bifida and anencephaly will be necessary to evaluate the effectiveness of folic acid fortification. (+info)
Comparison of thicknesses of the myocardial fibers of anencephalic and normal human fetuses.
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When heart transplantation is needed in newborns, brain death should be confirmed, and the heart should not be exposed to hypoxia. The anencephalic newborn has been presented as a donor in heart transplantation. It is important, therefore, to evaluate possible morphological differences in the hearts of anencephalic cases. In this study, muscle fibers were studied in 10 anencephalic and 10 normal fetuses (27-35 weeks) and the results were compared. Random samples were taken from the upper 1/3 of the right ventricle's posterior wall and processed for light microscopic examination. Thicknesses of the 100 myocardial muscle fibers for each fetus were evaluated. There was statistically no significant difference between the anencephalic and normal fetus groups and the sex groups. Morphological features of the transplant probably affects the performance of the heart after operation. The anencephalic fetuses could be unique donors for heart transplantation. (+info)
Ring chromosome 13: lack of distinct syndromes based on different breakpoints on 13q.
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A stillborn male child with anencephaly and multiple malformations was found to have the karyotype 46,XY,r(13) (p11q21.1). The breakpoint at 13q21.1, determined by high resolution banding, is the most proximal breakpoint ever reported in patients with ring chromosome 13. In situ hybridisation with the probe L1.26 confirmed the derivation from chromosome 13 and DNA polymorphism analysis showed maternal origin of the ring chromosome. Our results, together with a review of previous reports of cases with ring chromosome 13 with identified breakpoints, could neither support the theory of distinct clinical syndromes based on different breakpoints on 13q nor correlate the severity of symptoms with instability of the ring. (+info)
Neural tube defects associated with maternal periconceptional dietary intake of simple sugars and glycemic index.
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BACKGROUND: Maternal diabetes, prepregnancy obesity, hyperinsulinemia, and intakes of sweets have been associated with increased risks of neural tube defects (NTDs). The interdependence of these factors suggests a common pathogenesis via altered glycemic control and insulin demand. OBJECTIVE: We investigated whether maternal periconceptional dietary intakes of sucrose, glucose, fructose, and foods with higher glycemic index values influence the risk of having NTD-affected pregnancies. DESIGN: In a population-based case-control study, all hospitals in 55 of the 58 counties in California participated. In-person interviews were conducted with the mothers of 454 NTD cases (including fetuses and infants who were electively terminated, stillborn, or born alive) and with the mothers of 462 nonmalformed controls within an average of 5 mo from the term delivery date. The risk of having an NTD-affected pregnancy was the main outcome measure. RESULTS: Risks of having an NTD-affected pregnancy were not substantially elevated in relation to periconceptional intakes of glucose or fructose. Elevated risks of approximately 2-fold were observed for higher intakes of sucrose and foods with higher glycemic index values. Elevated risks were observed for high sucrose intake irrespective of whether adjustment was made for other covariates such as maternal folic acid intake. For higher glycemic index values, adjusted elevated risks of > or = 4-fold were observed in women whose body mass index (in kg/m(2)) was > 29. CONCLUSION: Our observed associations support observations that potential problems in glucose control are associated with NTD risk even among nondiabetic women. (+info)