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Biomedical subjects

F Stanley

Publications and source records attributed to F Stanley.

At least 37 records · Page 2Linked to original sources
PubMed1994

Why do aboriginal newborns weigh less? Gestational age at delivery: estimation, distribution and determinants.

We reviewed birth records pertaining to 1,301 Western Australian singleton Aboriginal pregnancies dated before 24 weeks by ultrasound fetometry using Caucasian standards. We compared i) ultrasound- and LMP-derived estimates of age at delivery for 323 pregnancies with available last menstrual period (LMP) dates and ii) distributions of ultrasound-estimated age at delivery for full-blood with part-blood Aboriginal neonates and with statutorily collected estimates for Caucasian neonates. We investigated determinants of age at delivery for Aboriginal neonates. Ultrasound-derived estimates of gestational age for Aboriginal pregnancies were statistically but not clinically significantly shorter than estimates derived from LMP dates claimed to be certain: mean difference = 0.4 weeks (95% CI:0.09-0.71). Aboriginal gestations were shorter than Caucasians' by 2 weeks (median) or 1 week (mode). Some shortening of gestation was accounted for by antepartum haemorrhage, congenital anomaly, history of syphilis, diabetes, hypertensive disease and inductions before 40 weeks without recorded medical complication but not by full-blood (relative to part-blood) Aboriginality. We conclude that Caucasian fetometry standards gave gestational estimates acceptably close to those derived from certain menstrual dates for dating scan before 24 weeks. Aboriginal gestations tended to be shorter than Caucasian gestations but since factors recorded in the medical record accounted for little of this difference, socioeconomic factors may be partly responsible.

Australia↗
PubMed1993

Twins, triplets, and cerebral palsy in births in Western Australia in the 1980s.

OBJECTIVES: To examine the rate of cerebral palsy in twins and triplets in births from 1980 to 1989 in Western Australia and to identify factors associated with increase in risk. DESIGN: Pluralities for all births in Western Australia were identified through the standardised midwives' notification system, and cases of cerebral palsy were identified from the Western Australian cerebral palsy register. MAIN OUTCOME MEASURES: Multiple births, cerebral palsy, excluding postneonatal cause. RESULTS: The prevalence of cerebral palsy in triplets, of 28 per 1000 survivors to 1 year (95% confidence interval 11 to 63) exceeded that in twins (7.3; 5.2 to 10) and singletons (1.6; 1.4 to 1.8). Although twins and triples were more likely than singletons to be low in birth weight, their risks of cerebral palsy if low in birth weight were similar. In contrast, in normal birthweight categories twins had a higher rate of cerebral palsy (4.2; 2.2 to 7.7) than singletons (1.1; 1.0 to 1.3). The prevalence of cerebral palsy was similar in twins of unlike sex pairs, all of whom are dizygotic, and in like sex pairs. A twin pair in which one member died in utero was at higher risk of cerebral palsy: 96 per 1000 twin pairs (36 to 218) compared with 12 (8.2 to 17) for twin pregnancies in which both survived. There was a similar but non-significant trend for death of one triplet to be associated with increased risk of cerebral palsy in the survivors of the set. CONCLUSION: Triplet pregnancies produced a child with cerebral palsy 47 times more often than singleton pregnancies did and twin pregnancies eight times more often. Eighty six per cent of cerebral palsy in multiple births was in twins. As multiple births are increasing mainly because of personal and medical decisions the increased risk of cerebral palsy in multiple births is of concern.

Birth Order↗
PubMed1993

When can cerebral palsy be prevented? The generation of causal hypotheses by multivariate analysis of a case-control study.

Causal hypotheses for spastic cerebral palsy were sought by comparing a population based sample of 183 cases with 549 matched controls. A time-ordered multivariate analysis was used to distinguish confounders and consequences of disease from possible causes, which could be single factors or sequences of factors. Eighteen factors were identified as having an association with spasticity that did not arise by confounding with other identified factors nor as a consequence of the disease. Nearly half the cases (48.6%) but only 14.4% of controls experienced one or more of these factors, but no one factor was experienced by > 11%, and most by < 5%, of cases. Those factors identified as occurring before labour commenced affected 35% of all cases. The proportion of cases experiencing identified factors and the distribution of those factors between epochs varied with gestation of delivery and with description and severity of impairment. The possible timing of causes in cases without identified factors and the role of preterm birth and poor intrauterine growth are discussed. We conclude that there were many pathways to spastic cerebral palsy many of which could not be identified. Each contributed only a small proportion and many may have been multifactorial. Intrapartum initiation of the aetiological pathway was relatively unimportant, being likely in about 9% of cases, but the majority of pathways commenced predelivery.

Adult↗
PubMed1993

Aetiological pathways to spastic cerebral palsy.

An aetiological pathway is a sequence of interdependent events culminating in disease. Recognition of such pathways can be clinically useful if it suggests more effective methods of disease prevention. Kernicterus arising from feto-maternal Rhesus incompatibility and resulting in choreoathetosis comprises an aetiological pathway to cerebral palsy. The failure to recognise sufficient causes or to intervene effectively when a sufficient cause is suspected in the majority of cerebral palsy cases suggests that there may be other aetiological pathways. Evidence for other pathways was sought in the data from the Western Australian case-control study of 183 children with spastic cerebral palsy. Two or more factors likely to be of aetiological significance were recognised for nearly one-third of cases. As anticipated, the numbers with any specific combination of factors were small, pointing to the need for collaborative studies to obtain larger numbers to confirm their aetiological significance. The implications for the true proportion of cases with multifactorial aetiology and the problems inherent in such an investigation are discussed.

Birth Injuries↗
PubMed1992

Birth defects in the infants of aboriginal and non-aboriginal mothers with diabetes in Western Australia.

OBJECTIVE: Because of the high prevalence of non-insulin-dependent diabetes in Australian Aborigines, and a suggestion that the prevalence of birth defects was high in the infants of Aboriginal mothers with gestational diabetes, this study was undertaken to determine the prevalence of birth defects in infants of Aboriginal and non-Aboriginal mothers with insulin-dependent, non-insulin-dependent, and gestational diabetes mellitus. DESIGN: A retrospective cohort study of all births to diabetic and non-diabetic mothers in Western Australia, 1980-1984. MAIN OUTCOME MEASURE: Birth defects diagnosed at any time up to the age of six years. RESULTS: Compared with infants of non-diabetic, non-Aboriginal mothers, the prevalence ratio for birth defects in infants of non-Aboriginal insulin-dependent mothers was 2.08 (95% confidence interval, 1.2-3.7), and for infants of mothers with non-insulin-dependent diabetes the ratio was 3.64 (95% CI, 1.5-8.6). The corresponding ratios for infants of Aboriginal mothers were 4.85 (95% CI, 0.8-28.2) and 3.64 (95% CI, 1.3-10.4). For birth defects in infants of gestational diabetic mothers, the prevalence ratio was 1.07 (95% CI, 0.6-1.9) for the non-Aboriginal group and 3.65 (95% CI, 2.3-6.0) for the Aboriginal group. Diabetes could have accounted for 0.14% of birth defects in infants of non-Aboriginal mothers and for 4.62% in infants of Aboriginal mothers. CONCLUSIONS: The excess of birth defects in infants of Aboriginal women with gestational diabetes may be due to non-insulin-dependent diabetes that predates the pregnancy but is only diagnosed during pregnancy. For Aboriginal infants, maternal diabetes may be the single most common known cause of birth defects that is amenable to change.

Cohort Studies↗
PubMed1992

Intrauterine growth and spastic cerebral palsy II. The association with morphology at birth.

This study tests the hypothesis that children with spastic cerebral palsy had different birth morphologies, defined in terms of their weight, length, head circumference, ponderal index and length to head circumference ratio, from that of the normal liveborn population. An earlier study showed a highly significant association of spastic cerebral palsy with low birthweight for gestational age in infants over 34 weeks gestation at delivery. This analysis defines morphological measurements as "abnormal" if not within the 10th-90th percentile ranges of appropriate total liveborn populations. The proportions with combinations of such measurements in 104 cases of spastic cerebral palsy from a population register of cerebral palsy are compared with those in a total liveborn population. Categories of 'abnormal' measurements associated with increased risk contained 44.4% of cases in excess of the proportion observed in the total population. More than half these excess cases were short for their gestation (suggesting size deficits originating before the 3rd trimester) and tended to have more severe forms of cerebral palsy. A further excess of 7.4% of cases had a head circumference above their 90th percentile: these generally developed mild cerebral palsy.

Birth Weight↗
PubMed1991

The aetiology of intellectual disability in Western Australia: a community-based study.

A register of intellectual disability is being established to assess the level and aetiology of intellectual disability in all children born and/or living in Western Australia. 1602 children aged between six and 16 years were identified who had IQs less than 70. 40 per cent had a definite genetic basis, 20 per cent an environmental cause and 40 per cent were of unknown aetiology. The insult was prenatal in 61 per cent, 10 per cent had a possible perinatal cause, 8 per cent were postnatal and for 21 per cent the timing could not be assessed. Approximately 20 per cent had concomitant cerebral palsy and 13 per cent were epileptic. A disparity was found between rural and urban areas, the prevalence being 9.9 and 6.5 per 1000 live births.

Adolescent↗
PubMed1990

Cerebral palsy in multiple births in Western Australia: genetic aspects.

A study of cerebral palsy in multiple births was undertaken to test genetic involvement and assess the impact of the special conditions of pregnancy and parturition in these cases. Complete ascertainment of cerebral palsy in multiple gestations that occurred in Western Australia between 1956 and 1985 was obtained from the Western Australian Cerebral Palsy Register. There were 74 twins and 5 triplets. Data on sex, birth order, motor handicap, outcome in co-twins and triplets, zygosity, and pedigree information was obtained from the Register, hospital records, and, where possible, by interview of the parent(s) of the propositi. There was a significantly higher (P = 0.0026) concordance rate in MZ than in DZ twin pairs. However, pedigree studies showed no other relatives with a motor handicap similar to that of the propositi. This is consistent with a multifactorial cause in at least some of the cases. The sex ratio of affected twins was found to be 2.1 compared to 1.3 for singletons and all 5 affected triplets were boys. The trend of increasing sex ratio with increasing plurality was significant at the 1% level.

Birth Order↗
PubMed1990

Intrauterine growth and spastic cerebral palsy. I. Association with birth weight for gestational age.

Birth weight, gestational age at delivery, and other factors were collected for 171 white children with spastic cerebral palsy. Their birth weights were compared with the birth weight distribution expected for a population of the same race, gestation, sex, maternal height, and parity, born in the same geographic area, and during the same time period. Birth weights of children with spastic cerebral palsy tended to be significantly lower than the median birth weight of their comparison population. Analysis stratified by gestation at delivery suggested that if the reduced birth weight were causally associated with the spastic cerebral palsy, 22% of cases were attributable to being below the 10th percentile of the comparison population birth weight distribution. The risk of spastic cerebral palsy associated with poor intrauterine growth was dependent on gestation at delivery; poorly grown infants delivered between 34 and 37 weeks' gestation were at highest risk. Some probable pathways by which growth retardation could result in brain damage (intrapartum hypoxia, hypoglycemia, and hypothermia) were investigated. Only intrapartum hypoxia may have played a causal role but probably accounted for less than 2% of all cases. These data suggest that spastic cerebral palsy is associated with poor intrauterine growth in infants of more than 33 weeks' gestation, but no important causal mechanism has yet been identified.

Birth Weight↗
PubMed1990

The homeodomain protein, Pit-1/GHF-1, is capable of binding to and activating cell-specific elements of both the growth hormone and prolactin gene promoters.

Studies were conducted to determine whether the trans-acting protein Pit-1/GHF-1 can bind to and activate promoter elements in both the GH and PRL genes that are necessary for cell-specific expression. Four pituitary cell lines that differentially express the endogenous GH and PRL genes were examined for their ability to activate GH and PRL promoter constructs containing sequences necessary for cell-specific expression (CSEs). Plasmids containing one CSE, -96 PRL and -104 GH, were similarly expressed in each of the four cell lines. Of the plasmids containing two CSEs, -173 PRL was always activated to a greater extent than -145 GH, with this relative activation being stronger in GC and GH1 cells than in 235-1 and GH4C1 cells. Protein-DNA binding assays were used to show that the GH and PRL CSEs specifically bound two highly abundant nuclear proteins (31 and 33 kDa). The two proteins were present at similar levels in all four pituitary cell lines and were recognized by a Pit-1/GHF-1 antibody. In contrast, HeLa and Rat2 cells did not activate transfected GH or PRL plasmids and did not contain nuclear proteins that specifically bound to the GH and PRL CSEs. However, cotransfection of these cells with the expression vector RSV-Pit-1/GHF-1 resulted in the activation of -173 PRL and -145 GH (PRL greater than GH). HeLa cells transfected with RSV-Pit-1/GHF-1 also contained 31- and 33-kDa nuclear proteins that bound to the GH and PRL CSEs. These results show that Pit-1/GHF-1 is present at levels in pituitary cell lines that are sufficient to activate the minimal elements in both the GH and PRL promoters necessary for cell-specific expression of these genes.

Animals↗
PubMed1989

Congenital malformations in aborigines and non-aborigines in Western Australia, 1980-1987.

A comparison of congenital malformations in Aboriginal and non-Aboriginal children in Western Australia has been made by means of data from the WA Congenital Malformations Registry, for births from 1980 to 1987 inclusive. Although the birth prevalence of all malformations was 3.5% for both Aboriginal and non-Aboriginal infants, significant differences were found in the birth prevalence of some individual malformations. Nervous-system and cardiovascular defects, and cleft lip and palate were significantly more prevalent in Aborigines, and pyloric stenosis and urogenital defects were significantly less prevalent. While some of the observed differences may have been a result of biases in ascertainment, others are likely to represent true differences. A discussion of Aboriginal beliefs concerning conception and birth is included, in order that the quantitative findings from the study might be considered in an appropriate cultural setting.

Congenital Abnormalities↗
PubMed1989

Transcriptional regulation of prolactin gene expression by thyroid hormone--alternate suppression and stimulation in different GH cell lines.

Transient expression experiments, using chimeric plasmids containing 3000 base pairs of PRL 5'-flanking sequences linked to the bacterial chloramphenicol acetyl transferase structural gene, demonstrate that L-T3 can inhibit (GH1 cells) or stimulate (GH4C1 cells) chloramphenicol acetyl transferase activity. Deletion experiments have defined the region necessary for these effects to sequences between -176 and -11 of the PRL gene. This region seems to contain the sequences necessary both for basal expression and for L-T3 regulation. Gel mobility shift experiments revealed that proteins extracted from GH1 and GH4C1 cell nuclei but not rat-2 fibroblasts interact with the PRL gene from -176 to +75. DNase I footprinting studies reveal two footprints which are the same in all pituitary derived cells tested. These footprints are not seen in rat-2 fibroblasts. Neither of these footprints likely represents binding of the L-T3-receptor since extracts from cells containing very low levels of receptor form footprints identical to those from cells with an abundance of receptors. These results suggest that different trans-acting factors, not identifiable by conventional footprinting techniques, are present in these cell lines which account for their opposite responses to L-T3. The regulation of PRL gene expression by L-T3 is unique in that both stimulation and suppression can be demonstrated using a single hormone-gene system. This should allow us to answer fundamental questions regarding the molecular switch between stimulation and suppression of gene expression by hormones.

Animals↗
PubMed1988

Stimulation of prolactin gene expression by insulin.

GH3 cells are a rat pituitary-derived cell line in which the expression of the growth hormone and prolactin genes is controlled by a variety of hormones including thyroid hormone. Since these cells contain insulin receptors, we explored whether these cells can be used to analyze the mechanisms involved in the regulation of gene expression by insulin. When GH3 cells were incubated with serum-free media, insulin stimulated prolactin production rates about 3-fold after 72 h and 10-fold after 96 h of incubation. Insulin stimulated prolactin mRNA levels and gene transcription rates to the same extent as the prolactin production rates. In contrast, insulin did not stimulate the rate of growth hormone production or growth hormone mRNA levels. As previously reported, thyroid hormone stimulated growth hormone production and mRNA levels. In these cells, thyroid hormone also stimulated prolactin synthesis and prolactin mRNA levels. Prolactin production and mRNA levels in cells incubated with both insulin and thyroid hormone showed a synergistic response which was about 5- to 10-fold greater than with either hormone alone. In contrast, growth hormone production rates in cells cultured with insulin and thyroid hormone was only slightly greater than cells incubated with only thyroid hormone. Half-maximal stimulation of prolactin production in cells incubated with insulin or with both insulin and thyroid hormone occurred between 2 and 5 nM insulin, suggesting that the response is mediated by the insulin receptor. These results indicate that GH3 cells should be useful in analyzing the mechanisms involved in regulation of gene expression by insulin.

Animals↗
PubMed1988

c-erbA protooncogenes mediate thyroid hormone-dependent and independent regulation of the rat growth hormone and prolactin genes.

Regulation of gene expression by the thyroid hormones is thought to be mediated by a nuclear-associated receptor found in a wide variety of cells and tissues. Cellular homologues of the avian erythroblastosis virus oncogene, v-erbA, encode proteins which bind thyroid hormone with similar affinities as thyroid hormone receptors. However, it has not been shown that any of the c-erbA proteins can function as receptor and modulate thyroid hormone responsive genes. In this study, using transient expression of chimeric reporter constructs, we document that the chick fibroblast c-erbA-alpha and the human placental c-erbA-beta modulate cis-acting regulatory sequences of two thyroid hormone responsive genes; rat GH and PRL. From these results we conclude: 1) in a receptor deficient cell line (235-1) both c-erbA subtypes act as hormone-dependent modulators of PRL gene expression and hence function as thyroid hormone receptors, 2) in two different receptor containing cell lines (GH4C1 and GH1), both c-erbA proteins act in a hormone-independent fashion to regulate PRL and GH expression. This suggests that events other than ligand binding can result in formation of a c-erbA protein that modulates transcription of thyroid hormone responsive genes, 3) no qualitative functional differences were detected between alpha- and beta-c-erbA subtypes, and 4) depending on the cell-type, L-T3 acts through its endogenous receptor to stimulate (GH4C1) or suppress (GH1) expression of a chimeric PRL construct. In these cells, c-erbA expression results in the same positive or negative response as the endogenous receptor except that the response occurs in the absence of hormone. These results suggest that the endogenous receptor and the c-erbAs act by augmenting the effect of transcription factors which can positively or negatively control gene expression.

Affinity Labels↗