Biomedical subjects
Publications and source records attributed to J Crane.
We report a case of status epilepticus lasting 5 h provoked by attempted self-hanging in a patient with no previous history of epilepsy. We are unable to find any published reports of status epilepticus being provoked in this manner.
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The present studies examine the various lymphotoxin (LT) forms released in vitro by phytohemagglutinin- (PHA) activated T-enriched (Te) human peripheral blood lymphocytes. It is clear that Te cells rapidly released (24 to 48 hr) these molecules in vitro. The 1st cell-lytic form detected in these supernatants is a 140-160,000 m.w. molecule(s) termed precursor alpha heavy (P alpha H). This form does not express alpha-LT antigenic determinants but is neutralized by antisera from animals injected with serum-free PHA-activated unseparated lymphocyte supernatants (anti-WS). The P alpha H is converted into alpha H, which expresses alpha determinants, by passage through molecular sieving columns or by treatment with low levels of Nonidet P-40 or urea. These treatments dissociate a small nontoxic 10-20,000 m.w. molecule(s), termed precursor factor (Pf), which masks the alpha-LT determinant on the P alpha H molecule. The dissociation of Pf is reversible, since alpha H from the molecular sieving columns will reassociate with the Pf. The alpha H LT class can further dissociate into the smaller alpha, beta, and gamma LT forms upon chromatography on a molecular sieving column, and a certain small percentage of the alpha H forms appear capable of associating to form the high m.w. complex (Cx) LT class. These findings suggest P alpha H may represent an intermediate that requires additional processing in order to proceed down 1 of 2 pathways: a) formation of complexes that are highly cell-lytic, or b) degradation by dissociation into the smaller weakly cell-lytic molecules identified as LT forms.
Little knowledge exists concerning long-term sequelae in children born of pregnancies complicated by chronic uteroplacental insufficiency. This follow-up study evaluates 12 children with positive contraction stress tests (CSTs) 5.5 months to 4.75 years following birth. Subsequent physical growth was uniformly normal in the four infants classified as appropriate for gestational age at birth; however, continued postnatal growth deficiency was present in 50% of the eight infants who suffered from intrauterine growth retardation. No major neurologic abnormalities were detected, and 10 of the 12 displayed normal mental and motor function, as determined by the Denver Developmental Screening Test, Bayley Scales of Infant Development and Wechsler Preschool and Primary Scale of Intelligence. Two of the 12 infants were depressed at birth and had serious neonatal complications. These were the only two children who scored poorly on the Bayley test. Although no conclusions regarding minimal brain dysfunction can be made, the majority of infants with positive CSTs demonstrate grossly normal neurologic and psychologic development.
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Thirty reports of partial 4p trisomy have been published. The manifestations and cytogenetic findings in four additional cases from two families are described in the present paper. Segregation analysis has been performed on the 21 families reported to date. The risk of having unbalanced offspring was the same in carrier mothers and carrier fathers. The risk of trisomic offspring was 14%. Among phenotypically normal progeny, normal karyotypes and balanced translocation states occurred with about equal frequency.
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To assess the relation between nicotine and cotinine levels in hair and reported exposure to environmental tobacco smoke (ETS), hair samples from 112 children (aged 3 months to 10 years) and 76 of their mothers were analyzed and information on the smoking habits of household adults in the preceding 6 months recorded. It was found that the levels of nicotine in children's hair were related to the number of smokers in the house, and increased with the total number of cigarettes smoked by all household adults (P<0.0001). In a multiple regression analysis, mother's smoking was much more a contributor to children's nicotine levels than smoking by the father or other household adults. Cotinine levels were less strongly associated with reported ETS exposure than nicotine. There was a strong correlation between nicotine hair levels in children and mothers (r(s)=0.7, P<0.0001). However, nicotine levels in the hair of active smokers were not correlated with the reported number of cigarettes they smoked per day. In this population, there was a consistent relation between exposure to ETS (assessed by questionnaire) and dose (as measured by nicotine in hair). We conclude that hair nicotine levels rather than hair cotinine levels provide an informative and objective measure of ETS exposure. The number of cigarettes smoked by active smokers may not be an accurate measure of the total nicotine levels in their bodies.
Hair nicotine levels were studied among children, relative to their caregivers' reported exposure to environmental tobacco smoke. A total of 117 children, aged 3 months to 10 years, were recruited consecutively from hospital inpatients, and their respective parents or caregivers were interviewed. Degree of exposure to environmental tobacco smoke was assessed via questionnaire. Scalp hair samples were collected from children and were assayed for nicotine. Levels of nicotine in hair among children reportedly exposed to smokers were higher than levels among unexposed children (chi2 = 26.46, p < .0001). In addition, hair nicotine levels were higher among children with mothers who smoked, compared with those whose mothers did not smoke. Whether household members smoked outside or inside the house had no significant effect on hair nicotine levels of children. Hair nicotine levels differed between children who were reportedly unexposed to environmental tobacco smoke at home and those who were exposed. Smoking outside the home, as reported by parents, did not cause a reduction in nicotine levels in the hair of children.
Diarrheal diseases are major causes of morbidity, with attack rates ranging from two to 12 or more illnesses per person per year in developed and developing countries. In addition, diarrheal illnesses account for an estimated 12,600 deaths each day in children in Asia, Africa, and Latin America. The causes of diarrhea include a wide array of viruses, bacteria, and parasites, many of which have been recognized only in the last decade or two. While enterotoxigenic Escherichia coli and rotaviruses predominate in developing areas, Norwalk-like viruses, Campylobacter jejuni, and cytotoxigenic Clostridium difficile are seen with increasing frequency in developed areas; and Shigella, Salmonella, Cryptosporidium species, and Giardia lamblia are found throughout the world. The rational management of infectious diarrhea requires the highly selective use of laboratory tests for these varied etiologic agents, depending on the clinical and epidemiologic setting. The purpose of this review is to provide an overview of the magnitude, special settings, and etiologies of diarrhea endemic to developed and developing countries. This information permits a practical approach to the diagnosis and management of common diarrheal illnesses in different settings.
OBJECTIVE: To describe and compare the body mass index (BMI; weight/height2) profile of 11-12-year-old children in Hawkes Bay, New Zealand in 1989 and 2000. To subsequently determine the prevalence of overweight and obesity at the two time points using international definitions. METHODOLOGY: As part of asthma prevalence studies in Hawkes Bay data on height, weight and ethnicity were collected from 871 school children in 1989, and 894 children in 2000 who reached 12 years of age during the year of testing. RESULTS: In the total study population the geometric mean BMI increased from 18.1 kg/m2 (95% CI 17.9; 18.3) in 1989 to 19.8 kg/m2 (95% CI 19.6; 20.0) in 2000, a relative increase of 9.2% (95% CI 7.6; 10.9), P < 0.001. Significant relative increases were found for males (9.0%: 95% CI 6.8; 11.3), females (9.3%: 95% CI 6.8; 11.8), Maori (7.6%: 95% CI 4.3; 11.1), European (9.1%: 95% CI 7.3; 11.0) and Pacific Island children (11.0%: 95% CI 2.2; 20.5). In 2000 20.9% of Hawkes Bay children were classified as overweight and 9.1% as obese. The risk of being overweight in 2000 was 2.2 times greater than the risk in 1989, and the risk of being obese was 3.8 times greater, with these problems more pronounced among Maori (overweight 24.7%, obese 15.3%) and Pacific Island (overweight 35.0%, obese 15.0%) than European (overweight: 18.2%, obese 5.7%) children. However, the risk of being overweight (RR = 3.0, 95% CI 2.2-4.0) or obese (RR = 8.3, 95% CI 3.0-23.3) in 2000 compared to 1989 was greater among European children. CONCLUSION: Higher percentages of Maori and Pacific Island children are overweight or obese compared to European, but in all ethnic groups there has been a statistically significant increase in mean BMI over an 11-year period. This increase reflects the trend observed in other developed countries and underlines childhood obesity as a major health problem in New Zealand.
BACKGROUND: The aetiological factors underlying the worldwide increase in the prevalence of asthma and the international patterns of the prevalence of asthma are not well understood. This has led to consideration of factors such as fetomaternal health which may programme the initial susceptibility to allergic sensitisation, or contribute to the development of asthma independently of sensitisation. METHODS: A number of epidemiological studies have examined the relationship between birth anthropometric measures (as a marker of fetomaternal health) and the subsequent development of asthma and atopy in childhood or adult life. RESULTS: Some, but not all of these studies have reported a relationship between enhanced fetal growth and an increased risk of asthma and/or atopy. CONCLUSION: These findings raise the hypothesis that factors responsible for fetal growth may also lead to programming of the developing respiratory or immune systems, predisposing to the subsequent development of asthma and/or atopy. This hypothesis may explain, in part, the increasing prevalence of asthma and atopy over recent decades, which has occurred concurrently with secular trends for improved fetomaternal health, as measured by anthropometric measurements at birth.
In response to the evidence that fenoterol was a major cause for the second epidemic of asthma deaths in New Zealand, the Department of Health severely restricted its availability, thereby allowing an 'experiment in prevention' to be undertaken. These regulatory actions, which effectively removed fenoterol from the market in New Zealand, were associated with a sudden and marked reduction in asthma mortality, providing further evidence for a causative role of fenoterol in the epidemic of asthma deaths in New Zealand.
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