Neonatal meningitis in England and Wales: a review of routine national data

The objective of this study was to describe trends in neonatal meningitis in England and Wales during the years 1975-91. Laboratory reports and, for the years 1983-91, data on statutory notifications and deaths from neonatal meningitis were reviewed. The mean annual total of laboratory reports of neonatal bacterial meningitis 1975-91 was 109 cases (range 69-133) with a slight upward trend apparent in the latter half of the study period. The mean annual number of reports of neonatal viral meningitis was only 14 cases with no trend apparent. The leading bacteria isolated were group B streptococci, Escherichia coli, and Listeria monocytogenes accounting for 34.1%, 28.5%, and 6.8% of reports, respectively. There was a change in the pattern of causative bacteria from 1981 onwards with the group B streptococcus displacing E coli as the leading cause. With respect to neonatal viral meningitis, echoviruses and coxsackie viruses accounted for 55.4% and 38.6% of cases, respectively. Neonatal meningitis was seriously undernotified; the ratio of laboratory reported cases to cases notified ranged from 12:1 in 1985 to 4:1 in 1989. The annual numbers of deaths ranged from 18 to 39. The laboratory reporting system provided the most useful data on secular trends and causative organisms for neonatal meningitis. The slight upward trend in the number of reports of bacterial meningitis merits continued surveillance.     

Oxygen consumption and evaporative water loss in infants with congenital heart disease

The relation between environmental temperature, heat production, oxygen consumption, and evaporative water loss was studied in 67 infants with congenital heart disease. The majority of the cyanosed infants had a low minimum oxygen consumption, a low evaporative water loss, and a diminished metabolic response to cold stress. Minimum oxygen consumption and evaporative water loss rose in 6 of these infants after the construction of a surgical shunt. Many of the ill acyanotic infants had an abnormally high minimum oxygen consumption, and those in cardiac failure often continued to sweat in an environment below the thermoneutral temperature zone.     

Making health data maps: a case study of a community/university research collaboration

This paper presents the main findings from a collaborative community/university research project in Canada. The goal of the project was to improve access to community health information, and in so doing, enhance our knowledge of the development of community health information resources and community/university collaboration. The project built on a rich history of community/university collaboration in Southeast Toronto (SETO), and employed an interdisciplinary applied research and action design. Specific project objectives were to: (1) develop via active community/university collaboration a geographic information system (GIS) for ready access to routinely collected health data, and to study logistical, conceptual and technical problems encountered during system development; and (2) to document and analyze issues that can emerge in the process of community/university research collaboration. System development involved iteration through community user assessment of need, development or refinement of the GIS, and assessment of the GIS by community users. Collaborative process assessment entailed analysis of archival material, interviews with investigators and participant observation. Over the course of the project, a system was successfully developed, and favorably assessed by users. System development problems fell into four main areas: maintaining user involvement in system development, understanding and integrating data, bringing disparate data sources together, and making use of assembled data. Major themes emerging from the community/university collaborative research process included separate community and university cultures, time as an important issue for all involved, and the impact of uncertainty and ambiguity on the collaborative process.     

The prevalence of hepatitis C in survivors of paediatric malignancy

Objective: To assess the prevalence of hepatitis C in 200 patients with paediatric malignancies, surviving in remission more than 5 years from diagnosis, who had received blood product transfusions before 1990 when routine screening of blood products for hepatitis C began.
Method: The second and third generation Abbott Diagnostics ELISA was used to assess hepatitis C seropositivity. Seropositive patients and those with abnormal liver transaminases were assessed by hepatitis C virus RNA polymerase chain reaction (PCR).
Results: A low incidence (4%) of seropositivity for hepatitis C was found in survivors of paediatric malignancy who were transfused prior to routine screening of blood products in this cohort.
Conclusions: All patients identified have evidence of hepatitis and may be at high risk of developing cirrhosis.     

Computed tomography changes following cryotherapy for hepatic cancer

Encouraging survival and tumour marker results have been described in patients where the focally destructive technique, hepatic cryotherapy, is used to treat primary and secondary hepatic malignancy. Radiology allows assessment of the cryotherapy procedure and follow-up treatment. This paper aims to review and describe the appearance of hepatic cryotherapy by CT.     

Dietary energy restriction does not inhibit pancreatic carcinogenesis by N-nitrosobis-2-(oxopropyl)amine in the Syrian hamster

Dietary energy restriction was previously shown to be effective in preventing a wide range of experimentally induced cancers. Studies were conducted to assess the influence on pancreatic carcinogenesis of dietary energy restrictions (reduced fat and carbohydrate) of 10%, 20% or 40% in comparison with control in Syrian hamsters treated with N- nitrosobis(2-oxopropyl)amine (BOP). Two carcinogenesis studies were conducted. One used a single treatment with 20 mg BOP/kg body weight and followed hamsters for 102 weeks following treatment, and the other used three weekly treatments of 20 mg BOP/kg body weight and followed hamsters for 45 weeks after treatment. Hamsters were fed control or energy restricted diet beginning the week following the last BOP treatment. Pancreatic carcinomas were induced in 9-18% of the hamsters in the first experiment and in 59-66% of the animals in the second. Dietary energy restriction did not influence carcinoma incidence in either study, and in the second experiment the multiplicity of tumors was higher in the 40% energy restriction (ER) group than in control hamsters. Plasma corticosterone was suppressed by BOP treatment, particularly in the 20% and 40% ER hamsters in the second experiment, and diet or BOP treatment did not significantly alter plasma cortisol. Pancreatic protein kinase Czeta measured by Western blot was highest in the cytosol and particulate fractions of the 40% ER hamsters in the first experiment. These results indicate that dietary energy restriction is not effective in the prevention of BOP induced pancreatic carcinogenesis in the Syrian hamster.      

Exposure to 60 Hz magnetic fields and risk of lymphoma in PIM transgenic and TSG-p53 (p53 knockout) mice

The results of a number of epidemiology studies suggest that exposure to power frequency (50 and 60 Hz) magnetic fields may be a risk factor for hematopoietic neoplasia. To generate experimental data to test this hypothesis, the influence of magnetic field exposure on lymphoma induction was determined in two strains of mice that are genetically predisposed to the disease. PIM mice, which carry the pim-1 oncogene, are highly sensitive to lymphoma induction by N-ethyl-N-nitrosourea (ENU); ENU-treated PIM mice were studied as a 'high incidence' lymphoma model. TSG-p53 (p53 knockout) mice, in which the p53 tumor suppressor gene has been deleted from the germ line, develop lymphoma as an age- related change; hemizygous TSG-p53 mice were studied as a 'low incidence' lymphoma model. Beginning 1 day after a single i.p. injection of 25 mg ENU/kg body wt, groups of 30 PIM mice/sex were exposed for 18.5 h/day to pure, linearly polarized, transient-free 60 Hz magnetic fields at field strengths of 0 (sham control), 0.02, 2.0 or 10.0 Gauss (G). An additional group of 30 PIM mice/sex was exposed intermittently (1 h on, 1 h off) to 10.0 G fields. Groups of 30 TSG-p53 mice/sex were exposed continuously to magnetic field strengths of 0 (sham control) or 10.0 G; TSG-p53 mice received no ENU. Studies were terminated after 23 weeks of magnetic field exposure. Lymphoma incidence in male PIM mice exposed continuously to 10.0 G magnetic fields was significantly reduced from that seen in sex-matched sham controls; survival, lymphoma incidence and lymphoma latency in other groups of PIM mice did not differ from sham controls. Survival and lymphoma incidence in all groups of TSG-p53 mice was 7% or less, regardless of magnetic field exposure regimen. These data do not support the hypothesis that exposure to magnetic fields is a significant risk factor for lymphoid neoplasia in mice with a genetic predisposition to the disease.      

Haplotype and interspersion analysis of the FMR1 CGG repeat identifies two different mutational pathways for the origin of the fragile X syndrome

To understand the origins of the fragile X syndrome and factors predisposing alleles to instability and hyperexpansion, we have compared the haplotype (using markers FRAXAC1, FRAXAC2, and DXS548) and AGG interspersion patterns of the FMR1 CGG repeat for 214 normal and 16 premutation chromosomes. Association testing between interspersion pattern and haplotype reveals a highly significant (P < 0.002) non- random distribution, indicating that all three markers are useful in phylogenetic reconstruction of mutational change. Parsimony analysis of the FMR1 CGG repeat substructure predicts that loss of AGG interruptions has occurred independently on many haplotypes associated with the fragile X syndrome, partially explaining the haplotype diversity of this disease. Among haplotypes found in linkage disequilibrium with the fragile X mutation, two different modes of mutation and predisposition to instability have been identified. One pathway has involved the frequent and recurrent loss of AGG interruptions from rare asymmetrical ancestral array structures. Intergenerational transmission studies suggest that these predisposed chromosomes progress relatively rapidly to the disease state. In contrast, the second mutational pathway involves a single haplotype which has maintained two AGG interruptions. Parsimony analysis of CGG repeat substructure within this haplotype suggests that larger alleles have been generated by gradual increments of CGG repeats distal to the most 3' interruption. Pedigree analysis of the intergenerational stability of alleles of this haplotype confirms a gradual progression toward instability thresholds. As a result, a large reservoir of chromosomes carrying large repeats on this haplotype exists. These chromosomes are predisposed to disease. The present data support a model in which there are at least two different mutational pathways predisposing alleles to instability and hyperexpansion associated with the fragile X syndrome.