Biomedical subjects

J Foley

Publications and source records attributed to J Foley.

At least 55 records · Page 3Linked to original sources

PubMed1996

Transactivation of the PTHrP gene in squamous carcinomas predicts the occurrence of hypercalcemia in athymic mice.

Humoral hypercalcemia of malignancy (HHM) is caused by the secretion of parathyroid hormone-related protein (PTHrP) by tumor cells, and tumors of squamous histology are the ones most commonly complicated by HHM. To determine why some squamous tumors cause HHM and others do not, we quantitated the levels of PTHrP mRNA expression and PTHrP secretion in a series of eight squamous tumor lines. As anticipated, we found that the level of PTHrP mRNA expression in individual lines correlated with their PTHrP secretion rates. However, PTHrP mRNA levels varied widely in individual lines, and only those tumor lines with the highest levels of PTHrP gene expression were able to cause hypercalcemia in athymic mice. We found that a specific segment of the PTHrP promoter could reproduce the relative pattern of PTHrP gene expression when cloned in front of a chloramphenicol acetyltransferase reporter gene and transiently transfected into these squamous lines. Deletional analysis confirmed that specific sequences within the PTHrP gene promoter appeared to be involved in the transactivation of the gene in tumor lines expressing high levels of PTHrP mRNA. These data suggest that the ability of a given squamous tumor to cause HHM is ultimately a function of its level of PTHrP gene expression, which in turn appears to be a function of the ability of specific transcription factors to transactivate PTHrP gene expression.

Animals↗

PubMed1996

CYP2J subfamily P450s in the lung: expression, localization, and potential functional significance.

Cytochrome P450 (P450) monooxygenases catalyze the epoxidation of arachidonic acid to form epoxyeicosatrienoic acids, which modulate bronchial smooth muscle tone and airway transepithelial ion transport. We recently described a new human P450 arachidonic acid epoxygenase (CYP2J2) and the corresponding rat homologue (CYP2J3). Northern analysis of lung RNA using CYP2J cDNA probes demonstrated that CYP2J2 and CYP2J3 mRNAs were expressed in the lung. Immunoblotting of microsomal fractions prepared from human and rat lungs using a polyclonal antibody raised against recombinant human CYP2J2 revealed a single 56-kDa band confirming abundant pulmonary CYP2J2 and CYP2J3 protein expression. Immunohistochemical analysis of formalin-fixed paraffin-embedded human and rat lung sections using the anti-human CYP2J2 IgG and avidin/biotin/peroxidase detection showed that CYP2J proteins were primarily expressed in ciliated epithelial cells lining the airway. Prominent staining was also noted in nonciliated airway epithelial cells, bronchial and pulmonary vascular smooth muscle cells, pulmonary vascular endothelium, and alveolar macrophages, whereas less intense staining was noted in alveolar epithelial cells. Endogenous epoxyeicosatrienoic acids were detected in both human and rat lung using gas chromatography/mass spectrometry, thus providing direct evidence for the in vivo human and rat pulmonary P450 metabolism of arachidonic acid. Based on these data, we conclude that CYP2J2 and CYP2J3 are abundant pulmonary arachidonic acid epoxygenases and that CYP2J products, the epoxyeicosatrienoic acids, are endogenous constituents of human and rat lung. In addition to known effects on airway smooth muscle tone and transepithelial electrolyte transport, the localization of CYP2J proteins to vascular smooth muscle and endothelium suggests that epoxyeicosatrienoic acids may also be involved in the modulation of pulmonary vascular tone.

8,11,14-Eicosatrienoic Acid↗

PubMed1996

Clonal variation of p53 expression and proliferative phenotype in A253 squamous carcinoma cells.

Loss of normal p53 tumor-suppressor gene function is characteristic of the majority of squamous carcinomas. During the course of gene transfer studies in the human squamous carcinoma cell line, A253, which does not express p53 mRNA or protein, we incidentally observed increased levels of p53 expression in up to 20% of clonal cell lines derived from parental A253 cells. p 53-expressing A253 cells (A253-p53) were also isolated by dilutional cloning. Nuclear p53 protein was identified by immunohistochemistry in A253-p53 cells in a wild-type pattern, and p53 mRNA (2.5 kb) was demonstrated by northern blot. Mutational analysis of the p53 gene in A253-p53 cells revealed no evidence for mutations in exons 5-9. A253-p53 cells could be distinguished from native A253 cells by prolonged doubling times (2-5 fold) and by a marked reduction of [3H]-thymidine uptake. Whereas A253 cells were unresponsive to the growth-inhibitory effects of TGF-beta, EGF-stimulated A253-p53 cells responded to TGF-beta with markedly reduced DNA synthetic rates. A253-p53 cells cocultured with A253 demonstrated enhanced cell growth and DNA synthesis rates compared to control A253-p53 cells. Finally, A253-p53 cells show reduced expression of c-fos, fibronectin, thrombospondin and parathyroid hormone-related protein (PTHrP) mRNAs. PTHrP measured by RIA in conditioned medium was approximately 300 pM for A253 but undetectable for A253-p53. We conclude that the A253 cell line contains a subpopulation of cells which express high levels of "wild-type-like" p53 protein. This results in dramatic changes in gene expression and a slower-growing phenotype in vitro.

Carcinoma, Squamous Cell↗

PubMed1995

Birth-weight ratio and cerebral palsy.

The birth-weight ratio, a convenient measure of fetal growth, has been used to assess the importance of antecedent and perinatal factors in a retrospective analysis of 605 cases of congenital cerebral palsy. All had been seen by the author at a special clinic over a period of three decades. The ratio (normally 1) is high in the very premature, falls in the middle of the third trimester, then begins to rise again at term. Abnormalities of pregnancy, or a history of maternal pregnancy-losses, depress the ratio perceptibly. In both singletons and twins, there is no significant relationship between a low ratio and the severity of the clinical condition, and presumably the extent of the brain damage. The findings suggest that growth retardation is an association and not a cause of perinatal vascular-anoxic lesions.

Abortion, Spontaneous↗

PubMed1995

Physicochemical and immunological characterization of the type E botulinum neurotoxin binding protein purified from Clostridium botulinum.

Type E botulinum neurotoxin is produced by Clostridium botulinum along with a neurotoxin binding protein which helps protect the neurotoxin from adverse pH, temperature, and proteolytic conditions. The neurotoxin binding protein has been purified as a 118-kDa protein. Secondary structure content of the neurotoxin binding protein as revealed by far-UV circular dichroism spectroscopy was 19% alpha-helix, 50% beta-sheets, 28% random coils, and 3% beta-turns. This compared to 22% alpha-helix, 44% beta-sheets, 34% random coils, and no beta-turns of the type E botulinum neurotoxin. The complex of the two proteins revealed 25% alpha-helix, 45% beta-sheets, 27% random coils, and 3% beta-turns, suggesting a significant alteration at least in the alpha-helical folding of the two proteins upon their interaction. Tyrosine topography is altered considerably (28%) when the neurotoxin and its binding protein are separated, indicating strong interaction between the two proteins. Gel filtration results suggested that type E neurotoxin binding protein clearly complexes with type E neurotoxin. The interaction is favored at low pH as indicated by an initial binding rate of 8.4 min-1 at pH 5.7 compared to 4.0 min-1 at pH 7.5 as determined using a fiber optic-based biosensor. The neurotoxin and its binding protein apparently are of equivalent antigenicity, as both reacted equally on enzyme-linked immunosorbent assay to polyclonal antibodies raised against the toxoid of their complex.

Animals↗

PubMed1995

Adolescents' misinterpretation of health risk probability expressions.

OBJECTIVE: To determine if differences exist between adolescents and physicians in their numerical translation of 13 commonly used probability expressions (eg, possibly, might). DESIGN: Cross-sectional. SETTING: Adolescent medicine and pediatric orthopedic outpatient units. PARTICIPANTS: 150 adolescents and 51 pediatricians, pediatric orthopedic surgeons, and nurses. MEASUREMENT: Numerical ratings of the degree of certainty implied by 13 probability expressions (eg, possibly, probably). RESULTS: Adolescents were significantly more likely than physicians to display comprehension errors, reversing or equating the meaning of terms such as probably/possibly and likely/possibly. Numerical expressions of uncertainty (eg, 30% chance) elicited less variability in ratings than lexical expressions of uncertainty (eg, possibly). CONCLUSION: Physicians should avoid using probability expressions such as probably, possibly, and likely when communicating health risks to children and adolescents. Numerical expressions of uncertainty may be more effective for conveying the likelihood of an illness than lexical expressions of uncertainty (eg, probably).

Adolescent↗

PubMed1994

The structure of the human peripherin gene (PRPH) and identification of potential regulatory elements.

We determined the complete nucleotide sequence of the coding region of the human peripherin gene (PRPH), as well as 742 bp 5' to the cap site and 584 bp 3' to the stop codon, and compared its structure and sequence to the rat and mouse genes. The overall structure of 9 exons separated by 8 introns is conserved among these three mammalian species. The nucleotide sequences of the human peripherin gene exons were 90% identical to the rat gene sequences, and the predicted human peripherin protein differed from rat peripherin at only 18 of 475 amino acid residues. Comparison of the 5' flanking regions of the human peripherin gene and rodent genes revealed extensive areas of high homology. Additional conserved segments were found in introns 1 and 2. Within the 5' region, potential regulatory sequences, including a nerve growth factor negative regulatory element, a Hox protein binding site, and a heat shock element, were identified in all peripherin genes. The positional conservation of each element suggests that they may be important in the tissue-specific, developmental-specific, and injury-specific expression of the peripherin gene.

Amino Acid Sequence↗

PubMed1994

Ras mutations in methylclofenapate-induced B6C3F1 and C57BL/10J mouse liver tumours.

The majority of genotoxic carcinogen-induced liver tumours of the sensitive B6C3F1 mouse contain activated H-ras oncogenes. Such mutations also occur in hepatocarcinogenesis-resistant strains. In order to determine whether this is true of non-genotoxic carcinogen-induced tumours, liver tumours induced in B6C3F1 and C57BL/10J mice by methylclofenapate (MCP) were compared. Polymerase chain reaction (PCR) analysis revealed H-ras codon 61 mutations in 11/46 B6C3F1 and 4/31 C57BL/10J liver tumours. The nude mouse tumorigenicity (NMT) assay was used to analyse tumours without codon 61 mutations. Of the 12 B6C3F1 liver tumour DNAs subjected to this assay, one contained a H-ras codon 117 mutation. Further PCR analysis on frozen tumour samples (46 B6C3F1 and 15 C57BL/10J) revealed no codon 12 mutations; one additional codon 117 mutation was identified in a B6C3F1 tumour. Overall, then, H-ras codon 61 mutations were detected in MCP-induced B6C3F1 tumours less frequently than in genotoxin-induced tumours. Two B6C3F1 tumours contained codon 117 mutations similar to those previously found in tumours induced by ciprofibrate, furan and furfural, and in at least one spontaneous tumour. Ras mutations were also detected in some C57BL/10J tumours, providing further evidence that ras oncogenes can participate in hepatocarcinogenesis in resistant mice.

Alleles↗

PubMed1994

Expression of the neural intermediate filament proteins peripherin and neurofilament-66/alpha-internexin in neuroblastoma.

BACKGROUND: Peripherin and neurofilament (NF)-66/alpha-internexin are recently characterized, neuron-specific intermediate filament proteins that are expressed in the developing peripheral nervous system. Peripherin, in particular, is highly enriched in neuronal derivatives of the neural crest. We speculated that these intermediate filament proteins would be expressed in neuroblastoma (NB), a neural crest-derived tumor with many neuronal features. EXPERIMENTAL DESIGN: By use of antibodies specific to peripherin and NF-66/alpha-internexin, we detected these proteins on Western blots of NB tissue extracts and in paraffin sections of NBs. RESULTS: Western blotting indicated that NB tumor extracts contained immunoreactive proteins that co-migrated with rat peripherin and human NF-66/alpha-internexin from normal tissues, thus establishing the specificity of the antibodies for these proteins in tumors. The antibody specific for peripherin labeled all NBs, including immature NBs, composite ganglioneuroblastomas and ganglioneuromas. In contrast, the NF-66/alpha-internexin antibody labeled only 50% of NBs, and only weakly labeled most ganglioneuroblastomas and ganglioneuromas. Neither antibody labeled other small blue cell tumors such as lymphomas, rhabdomyosarcomas, Wilms' tumors, and Ewing sarcomas. CONCLUSIONS: The specificity of the peripherin labeling of NB and the ability of the peripherin antibody to label the entire spectrum of NBs, including ganglioneuroblastomas and ganglioneuromas, indicate that this intermediate filament protein has potential as a diagnostic marker for these related neural crest neoplasms.

Animals↗

PubMed1993

Parental age, genetic mutation, and cerebral palsy.

Parental age and birth order were studied in 251 patients with cerebral palsy. No parental age or birth order effects were observed in spastic quadriplegia or diplegia, but a paternal age effect was detected in those with athetoid/dystonic cerebral palsy and congenital hemiplegia. These observations indicate that some cases of athetoid/dystonic or hemiplegic cerebral palsy might arise by fresh dominant genetic mutation.

Adolescent↗

PubMed1993

Comparison of proliferating cell nuclear antigen to tritiated thymidine as a marker of proliferating hepatocytes in rats.

Proliferating cell nuclear antigen (PCNA), an endogenous nuclear protein, has recently been used to identify replicating cells. PCNA was compared to tritiated thymidine ([3H]-TdR), a reliable and accurate exogenous labeling agent, to ascertain if PCNA gives comparable results for quantitative cell proliferation. Male F344 rats were treated with a single dose of 500 mg/kg 4-acetylaminofluorene (4-AAF), a known liver mitogen. Rats (n = 5) were euthanized and necropsied at 6, 12, 18, 24, 36, 48, 96, or 192 hr after treatment. Two hours before necropsy, rats were pulsed-dosed with [3H]-TdR (2 mCi/kg body weight). Livers were sectioned, autoradiography performed, and labeling indexes (LI), a measurement of the percentage of S-phase hepatocytes, determined. One and a half years after the completion of this study, the archival paraffin blocks of the liver tissue were sectioned and stained for PCNA by an immunohistochemical procedure. Immunocytochemical staining patterns of proliferating cell nuclear antigen antigen expression permitted the recognition of G1, S, G2, M, and quiescent cells. PCNA LI, generated by scoring only cells exhibiting S-phase staining patterns, was compared to the pulse [3H]-TdR LI for each animal. Similar periportal staining patterns of S-phase nuclei were detected by both markers. The [3H]-TdR LI and the PCNA LI exhibited a peak at 24 hr of approximately the same magnitude. However, while the [3H]-TdR LI had returned to near baseline at the 48-hr time point, the PCNA LI remained elevated until the 96-hr time point. This sustained elevation of the PCNA index cannot be explained at this time.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Acetylaminofluorene↗

PubMed1993

Sources of health insurance and characteristics of the uninsured. Analysis of the March 1992 Current Population Survey.

Eighty-three percent of nonelderly Americans and 99 percent of elderly Americans (aged 65 and over) were covered by either public or private health insurance in 1991, according to EBRI tabulations of the March 1992 Current Population Survey (CPS). The March 1992 CPS is the most recent data available on the number and characteristics of uninsured Americans. In 1991, 16.6 percent of the nonelderly population--or 36.3 million people--were not covered by private health insurance and did not receive publicly financed health assistance. This number compares with 35.7 million in 1990 (16.6 percent), 34.4 million in 1989 (16.1 percent), and 33.6 million in 1988 (15.9 percent). The most important determinant of health insurance is employment. Nearly two-thirds (64 percent) of the nonelderly have employment-based coverage. Workers were much more likely to be covered by group health plans than nonworkers (71 percent versus 40 percent). Even though workers and members of their families were more likely to be covered by health insurance than nonworkers, 85 percent of the uninsured lived in families headed by workers in 1991, primarily because most people lived in families headed by workers. More than 60 percent of uninsured were in families headed by full-year workers with no unemployment. Nearly all persons who were covered by an employment based-plan received at least some contribution to that plan from their employer. The estimated average annual contribution among those receiving a contribution to employee or family plans was $2,129. Although many individuals in poor families are covered by public health plans, that coverage is far from universal. In 1991, only 52 percent of the nonelderly with income below the poverty line were covered by a public plan--49 percent by Medicaid. The number of children who were uninsured in 1991 was 9.5 million, or 14.7 percent of all children, compared with 9.8 million or 15.3 percent of all children in 1990. Twenty-three percent of children were covered by public health insurance, with 21 percent being covered by Medicaid. In 11 states and the District of Columbia, more than 20 percent of the population was uninsured in 1991. These states and their uninsured rates were the District of Columbia (30.3 percent), Texas (25.3 percent), New Mexico (24.5 percent), Louisiana (23.8 percent), Florida (23.5 percent), Mississippi (22.1 percent), Oklahoma (22.1 percent), Nevada (21.8 percent), California (21.7 percent),Arizona (21.1 percent), Alabama (20.6 percent), and Idaho (20.6 percent).

Adult↗

PubMed1993

Flexible benefits, choice, and work force diversity.

This Issue Brief evaluates the prevalence of flexible benefits plans and their ability to achieve cost management goals and to meet the needs of diverse employee groups. In addition, it examines flexible benefits plans' current legislative and regulatory status and typical plan design features. Sec. 125 of the Internal Revenue Code allows employers to provide employees with a choice among benefits, including moving otherwise taxable cash compensation to the pre-tax purchase of benefits, without requiring them to include the value of the noncash benefits in their adjusted gross income unless they choose taxable options. Although the percentage of full-time employees in medium and large private establishments who are eligible for cafeteria plans has not increased appreciably, the percentage of employees eligible for freestanding flexible spending accounts (FSAs) nearly tripled between 1988 and 1991. Generally, the proportion of employers sponsoring cafeteria plans or FSAs increases with employer size. Recent surveys show that 27 percent of employers with 1,000 or more employees offered choice-making plans in 1991, 48 percent of firms offered health care FSAs, and 54 percent offered dependent care FSAs, either in conjunction with cafeteria plans or as a stand-alone option. Ten percent of full-time employees in private firms employing 100 or more workers were eligible to participate in cafeteria plans in 1991. Only 5 percent of full-time employees in state and local governments and 1 percent of similar employees in small private establishments were eligible for cafeteria plans in 1990. Recent Bureau of Labor Statistics' surveys show that, among full-time employees, 27 percent in private establishments with 100 or more employees, 28 percent in state and local governments, and 6 percent in small private establishments were eligible to participate in freestanding FSAs. In 1992, 21 percent of eligible employees contributed to a health care FSA, and only 3 percent of eligible employees contributed to a dependent care FSA. Contributions to health care FSAs averaged $651, and those to dependent care FSAs averaged $2,959. National health reform could have a significant impact on these plans if the tax treatment of health benefits is changed. Taxation of health benefits in excess of a standard benefits package would fundamentally reduce the ability to use FSAs.

Community Participation↗

PubMed1993

The role of the health care sector in the U.S. economy.

This Issue Brief discusses factors that contribute to the growth of health care expenditures and the reasons that many individuals, employers, and policymakers consider health expenditures too high. In addition, it describes various industries that make up the health care delivery system and their role in the U.S. economy as employers, producers, exporters, and suppliers of research and development. The report also discusses the economic implications of rising health care expenditures for individuals, employers, and the federal government and the potential impact of proposed health care reform on the health care sector and the U.S. economy as a whole. Health care delivery industries such as pharmaceuticals and medical equipment suppliers have higher than average research and development levels, in addition to a positive balance of trade. Moreover, while the total number of jobs in the private sector declined between 1990 and 1993, the number of jobs in the relatively high paid health services sector continued to grow. In aggregate, employer spending on health care represents only 6.6 percent of total labor costs. In comparison, wages and salaries represent 83 percent of total labor costs. Consequently, the growth rate of health care expenditures has a smaller impact on the growth rate of total compensation than does the growth rate in wages and salaries. Using job multipliers developed by the U.S. Department of Commerce, it is estimated that the 18,600 health care services jobs in Rochester, Minnesota in 1993 created another 32,000 jobs in the area. Any contraction of the health care sector in cities that have a large concentration of employment in health services would result in reduced employment in restaurants, retail stores, janitorial services, and other local businesses. EBRI's simulations estimated that between 200,000 and 1.2 million workers could become unemployed as a direct result of a mandate that employers provide health benefits to their employees, assuming that wages and salaries did not adjust at all. Others find that approximately 50,000 individuals would lost their jobs, assuming that wages and other labor costs adjust downward to completely account for increased costs. As is apparent, the estimates of job loss (and of the total costs of the policy) are extremely sensitive to the assumptions used in the simulation.

Commerce↗

PubMed1992

DNA methylation inhibits transcription of procollagen alpha 2(I) promoters.

Our previous studies have demonstrated that a 2-[N-(acetoxyacetyl)amino]fluorene-transformed rat epithelial-like cell line, W8, contains a transcriptionally inactive alpha 2(I) gene with a hypermethylated promoter/first-exon region. We have cloned the rat promoter/first-exon region (-211 to +207) from W8 cells and their parent cell line, K16, which expresses alpha 2(I) collagen. There were no sequence differences between the clones from the two cell lines, indicating that a mutation was not responsible for transcriptional inhibition. The alpha 2(I) rat promoters were cloned upstream of the chloramphenicol acetyltransferase gene. Both constructs were equally active in both cell lines, suggesting that trans-activating factors for alpha 2(I) transcription are present in W8 cells. Finally, methylation of plasmids at all CpG sites with SssI methylase completely inhibited transcription using alpha 2(I) promoters, but methylation did not inhibit simian-virus-40 promoter-driven transcription. Certain methylation sites partially inhibit promoter activity. An HhaI methylation site inhibited transcriptional activity of the alpha 2(I) promoter 8-fold, whereas methylation at the HpaII site in the rat alpha 2(I) promoter did not decrease transcriptional activity. This provides further evidence that methylation at specific sites in the collagen alpha 2(I) promoter is responsible for the inactivation of transcription in W8 cells.

Animals↗

PubMed1992

Proto-oncogene activation in liver tumors of hepatocarcinogenesis-resistant strains of mice.

Activation of the ras family of oncogenes occurs frequently in liver tumors of the B6C3F1 mouse, a strain which is highly sensitive to hepatocarcinogenesis. Many other mouse strains are much more resistant to hepatocarcinogenesis; the aim of this study was to determine the frequency and pattern of oncogene activation in spontaneous and chemically induced liver tumors of three such strains, the C57BL/6J, the C57BL/6 x DBA/2 F1 hybrid (B6D2F1) and the C57BL/6 x Balb/c F1 hybrid (B6BCF1). The C57BL/6, DBA/2 and Balb/c strains are all relatively resistant to spontaneous hepatocarcinogenesis (1.5-3.6% of animals develop liver tumors in 2 years); with regard to chemically induced hepatocarcinogenesis the Balb/c is highly resistant, the C57BL/6 has low susceptibility and the DBA/2 has low to moderate susceptibility. The nude mouse tumorigenicity assay was used to search for activated oncogenes in 15 C57BL/6J liver tumors induced by a single neonatal dose of vinyl carbamate (VC, 0.15 mumol/g body weight). Three tumors contained H-ras genes activated by point mutations at codon 61 and one contained a non-ras oncogene. The polymerase chain reaction and allele-specific oligonucleotide hybridization were used to study H-ras mutations in spontaneous and VC-induced tumors from all three strains of mice. The frequency of H-ras codon 61 mutations in tumors induced by 0.15 mumol/g body weight VC in the C57BL/6J mouse (5/37) was similar to that in spontaneous tumors (2/9); surprisingly, tumors induced by a lower dose of VC (0.03 mumol/g body weight) had a higher frequency of H-ras mutations (12/28). The frequencies of H-ras activation detected in VC (0.03 mumol/g body weight)-induced tumors from the two F1 hybrids studied differed markedly. Only one VC-induced B6BCF1 tumor contained a mutated H-ras gene (1/10), whereas the majority of B6D2F1 tumors contained such mutations (23/33). Several spontaneous B6D2F1 liver tumors contained H-ras codon 61 mutations (6/15). Thus, H-ras activation frequency does not determine susceptibility to hepatocarcinogenesis in inbred mice and their F1 hybrids, since a relatively high frequency of H-ras mutations was observed in two resistant strains and a low frequency was found in the other strain.

3T3 Cells↗

PubMed1992

The offspring of people with cerebral palsy.

To test a hypothesis that a placental deficit as a possible cause of CP might be transmitted, 88 people with congenital CP were contacted by questionnaire and letters. They had had 122 children, 93 per cent of whom were reported to be normal. The frequency of miscarriages and toxaemia was normal. 5 per cent of the mothers had had emergency caesarean sections. Three mothers also had minor malformations. The mean gestational age of the children was 38.8 weeks and their mean birthweight was 3295g. The mean birthweight of the mothers born preterm was 984g and that of their babies was 3244g. Two of the 122 children had diplegia, four had malformations, one had trisomy 18 and there was one stillbirth.

Adolescent↗

PubMed1992

Dyskinetic and dystonic cerebral palsy and birth.

Two hundred and nineteen cases of the dyskinetic and dystonic forms of cerebral palsy which were seen in the course of three decades at a single clinic have been analysed. Fifty-seven patients had kernicterus. In the remaining 162, 71% of whom were born at term, birthweight was below the expected mean in two-thirds. There was no relationship between birth weight, or abnormal birth, or asphyxia, and the ultimate clinical severity of the children. We conclude that abnormal birth and asphyxia are not direct causes of the cerebral damage, but are expressions of a pre-existing condition resulting in susceptibility to the stress of birth, whether it is normal or abnormal.

Adult↗