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K Gardiner

Publications and source records attributed to K Gardiner.

At least 19 recordsLinked to original sources
PubMed2003

What is the problem with breast-feeding? A qualitative analysis of infant feeding perceptions.

AIMS AND OBJECTIVES: Breast-feeding rates are low in Northern Ireland (NI) compared with other regions of Europe. The aim of this study has therefore been to define and explore factors determining infant feeding decisions with a view to the planning of future research and intervention needs. METHOD: Participants were approached at convenience from the throughput of women attending a large teaching hospital antenatal clinic to take part in focus group discussion. RESULTS: Dominant themes indicated that the main barriers to breast-feeding are restricted freedom and independence associated with family issues, return to work, societal embarrassment and perceived social isolation. The dialogue suggested that breast-feeding leads to inability to carry out everyday activities and social exclusion. CONCLUSIONS: Incompatible social norms make it difficult for mothers to breast-feed successfully. This implies that future promotional efforts should take a societal approach.

Adult↗
PubMed2003

Pneumatosis coli, a benign form of necrotising enterocolitis.

Necrotising enterocolitis (NEC) is the most common acquired gastrointestinal emergency in neonates. Presence of pneumatosis intestinalis is taken as evidence of definite NEC. A distinctive but rare form of NEC called "pneumatosis coli" has been described, presenting with gross blood in stools and minimal or absent local and systemic signs. Radio-graph characteristically reveal isolated colonic pneumatosis without small bowel involvement. Pneumatosis coli has a more benign course compared with definite NEC. Total parenteral nutrition, antibiotics, an appropriate duration off feeds and close observation remain the corner stones of therapy assuring a benign course.

Colonic Diseases↗
PubMed2002

Phylogenetic comparison of the pre-mRNA adenosine deaminase ADAR2 genes and transcripts: conservation and diversity in editing site sequence and alternative splicing patterns.

Adenosine deaminase that acts on RNA -2 (ADAR2) is a member of a family of vertebrate genes that encode adenosine (A)-to-inosine (I) RNA deaminases, enzymes that deaminate specific A residues in specific pre-mRNAs to produce I. Known substrates of ADAR2 include sites within the coding regions of pre-mRNAs of the ionotropic glutamate receptors, GluR2-6, and the serotonin receptor, 5HT2C. Mammalian ADAR2 expression is itself regulated by A-to-I editing and by several alternative splicing events. Because the biological consequences of ADAR2 function are significant, we have undertaken a phylogenetic comparison of these features. Here we report a comparison of cDNA sequences, genomic organization, editing site sequences and patterns of alternative splicing of ADAR2 genes from human, mouse, chicken, pufferfish and zebrafish. Coding sequences and intron/exon organization are highly conserved. All ADAR2 genes show evidence of transcript editing with required sequences and predicted secondary structures very highly conserved. Patterns and levels of editing and alternative splicing vary among organisms, and include novel N-terminal exons and splicing events.

Adenosine Deaminase↗
PubMed2002

Longitudinal analyses of chest radiographs from the European Carbon Black Respiratory Morbidity Study.

High levels of exposure to carbon black have been linked with an increased prevalence of chest radiograph abnormalities. However, it is unclear to what extent current levels of exposure in the carbon black manufacturing industry are associated with new cases of and progression in small opacities. Longitudinal analyses were carried out on data from workers in the European carbon black manufacturing industry who provided three full-size chest radiographs sequentially between 1987-1995. All chest radiographs were independently read by three experienced readers according to the International Labour Organisation (ILO) classification. After exclusion of participants with previous lung diseases or injuries, females, unreadable chest radiographs and from factories with a low participation rate, data from 675 workers were available for the longitudinal analyses. An association was observed between cumulative carbon black exposure and new cases of chest radiograph abnormalities (ILO category > or = 1/0) and progression in small opacities. These associations were mainly related to changes in chest radiographs from workers at one factory. A large percentage of workers with chest radiograph abnormalities reversed to normal chest films; however, after adjusting for other factors, this was not associated with levels of exposure to carbon black dust. In conclusion, the results show that exposure to carbon black is associated with increased risk of chest radiographic abnormalities, which may be reversible after reduction or cessation of exposure.

Administration, Inhalation↗
PubMed2001

Full-sized HERV-K (HML-2) human endogenous retroviral LTR sequences on human chromosome 21: map locations and evolutionary history.

One of the evolutionary mechanisms for acquisition of novel functional sequences can be domestication of exogenous retroviruses that have been integrated into the germ line. The whole genome mapping of such elements in various species could reveal differences in positions of the retroviral integration and suggest possible roles of these differences in speciation. Here, we describe the number, locations and sequence features of the human endogenous retrovirus HERV-K (HML-2) long terminal repeat (LTR) sequences on human chromosome 21. We show that their distribution along the chromosome is not only non-random but also roughly correlated with the gene density. Amplification of orthologous LTR sites from a number of primate genomes produced patterns of presence and absence for each LTR sequence and allowed determination of the phylogenetic ages and evolutionary order of appearance of individual LTRs. The identity level and phylogenetic age of the LTRs did not correlate with their map locations. Thus, despite the non-random distribution of LTRs, they have apparently been inserted randomly into the chromosome relative to each other. As evidenced in previous studies of chromosomes 19 and 22, this is a characteristic of HERV-K integration.

Animals↗
PubMed2001

A cohort mortality study of U.K. carbon black workers, 1951-1996.

BACKGROUND: Carbon black, a powdered form of elemental carbon is used in the manufacture of rubber products, paints, plastics, and inks. In 1974, the Health and Safety Executive initiated a cohort mortality study on possible carcinogenic effects on carbon black workers. METHODS: The mortality of a cohort of 1,147 male manual workers from five U.K. factories manufacturing carbon black was investigated for the period 1951-1996. All subjects were employed in the carbon black industry for 12 months or more, and all were first employed before 1975. Limited work histories were used to calculate estimates of individual cumulative exposure to carbon black, using a job-exposure matrix derived by the study team. RESULTS: Based on serial rates for the general population of England and Wales, significantly elevated mortality was observed in the main study cohort for all causes (Obs 372, Exp 328.7, SMR 113, P < 0.05) and for lung cancer (Obs 61, Exp 35.3, SMR 173, P < 0.001). There were highly elevated lung cancer SMRs at two of the factories, and unexceptional SMRs at the remaining three factories. There was no indication of lung cancer SMRs increasing with period from first employment. Poisson regression analyses failed to find significant trends of lung cancer risks increasing either with cumulative exposure to carbon black (4 levels) or with duration of employment at the participating factories (4 levels). CONCLUSIONS: Confident interpretation of the elevated SMRs found for lung cancer in two of the factory subcohorts is not possible but the study has been unable to link cumulative exposure to carbon black with elevated risks of lung cancer.

Adult↗
PubMed2001

Evolutionary breakpoints on human chromosome 21.

Segments of the long arm of human chromosome 21 are conserved, centromere to telomere, in mouse chromosomes 16, 17, and 10. There have been 28 genes identified in human chromosome 21 between TMPRSS2, whose orthologue is the most distal gene mapped to mouse chromosome 16, and PDXK, whose orthologue is the most proximal gene mapped to mouse chromosome 10. Only 6 of these 28 genes have been mapped in mouse, and all are located on chromosome 17. To better define the chromosome 17 segment and the 16 to 17 transition, we used a combination of mouse radiation hybrid panel mapping and physical mapping by mouse: human genomic sequence comparison. We have determined the mouse chromosomal location of an additional 12 genes, predicted the location of 7 more,and defined the endpoints of the mouse chromosome 17 region. The mouse chromosome 16/chromosome 17 evolutionary breakpoint is between human genes ZNF295 and UMODL1, showing there are seven genes in the chromosome 16 segment distal to Tmprss2. The chromosome 17/chromosome 10 breakpoint seems to have involved a duplication of the gene PDXK, which on chromosome 21 lies immediately distal to the KIAA0179 gene. These data suggest that there may be as few as 21 functional genes in the mouse chromosome 17 segment. This information is important for defining existing and constructing more complete mouse models of Down syndrome.

Animals↗
PubMed2001

Genomic sequence analysis tools: a user's guide.

The wealth of information from various genome sequencing projects provides the biologist with a new perspective from which to analyze, and design experiments with, mammalian systems. The complexity of the information, however, requires new software tools, and numerous such tools are now available. Which type and which specific system is most effective depends, in part, upon how much sequence is to be analyzed and with what level of experimental support. Here we survey a number of mammalian genomic sequence analysis systems with respect to the data they provide and the ease of their use. The hope is to aid the experimental biologist in choosing the most appropriate tool for their analyses.

Internet↗
PubMed2001

Determinants of inhalable dust exposure in the European carbon black manufacturing industry.

A large study to investigate the respiratory health effects of occupational exposure to carbon black in the European carbon black manufacturing industry commenced in 1987. During the study, a large amount of personal occupational exposure data was collected. This article describes the empirical models used to study the determinants of inhalable dust exposure, using data from 16 factories collected in the third and last cross-sectional phase of this study. Information on activities during the measurements was collected using short job category-specific questionnaires. In addition, questionnaires were completed by factory representatives on the implementation of control measures and changes in production process since the first cross-sectional phase. Mixed effects analyses of variance models were used to identify determinants of exposure, while taking into account the within- and between-worker (random) variance components. The results of these models show that, for any job category, factory is a strong predictor of exposure in this industry. These differences could not be explained entirely by factors such as age of the factory or the control measures implemented since the first phase of the study. Surprisingly, implementation of local exhaust ventilation systems had an effect that was counterintuitive; for example, in warehouses where local exhaust ventilation systems had been implemented, higher dust exposure levels were found compared to those where such control measures had not been installed since the first cross-sectional survey. Season appeared to have some effect on exposure for some job titles, with generally relatively low exposures being found in the summer. Finally, a number of activities were identified that caused higher levels of dust exposure, most notably "changing of filters" and "clean-up of carbon black spills."

Air Pollutants, Occupational↗
PubMed2001

Respiratory health effects from exposure to carbon black: results of the phase 2 and 3 cross sectional studies in the European carbon black manufacturing industry.

OBJECTIVES: To assess respiratory morbidity over several cross sectional phases in the European carbon black manufacturing industry. METHODS: Participants completed an amended (and translated) MRC respiratory morbidity questionnaire with additional questions on previous exposures, job history, etc, and spirometry traces in each phase. Concurrent with the health outcome measures, personal exposure to inhalable dust was measured. RESULTS: Percentage participation rose from 90% in phase 2 (19 factories) to 95% in phase 3 (16 factories). Exposure dropped slightly between the 2 and 3 phases; as did the prevalence of reporting symptoms. Percentage of predicted lung function volumes exceeded 100% for forced expired volume in 1 second (FEV(1)) and forced vital capacity (FVC), whereas forced mid-expiratory flow (FEF(25%-75%)) and FEV(1)/FVC ratio were below 100% in both phases. The multiple linear and logistic regressions showed that carbon black had a significant effect on lung function and on most respiratory symptoms, respectively. CONCLUSION: Both current and cumulative exposure to carbon black have a deleterious effect on respiratory morbidity. Due to the drop in exposure between phases 2 and 3, recent exposures seem to have less of an impact on the respiratory morbidity in the workers in phase 3 than those in phase 2.

Air Pollutants, Occupational↗
PubMed2001

Ts65Dn -- localization of the translocation breakpoint and trisomic gene content in a mouse model for Down syndrome.

Fluorescent in situ hybridization (FISH) -- using mouse chromosome paints, probes for the mouse major centromeric satellite DNA, and probes for genes on chromosomes (Chr) 16 and 17 -- was employed to locate the breakpoint in a translocation used to produce a mouse model for Down syndrome. The Ts65Dn trisomy is derived from the reciprocal translocation T(16;17)65Dn. The Ts65Dn mouse carries a marker chromosome containing the distal segment of Chr 16, a region that shows linkage conservation with human Chr 21, and the proximal end of Chr 17. This chromosome confers trisomy for most of the genes in the Chr 16 segment and Ts65Dn mice show many of the phenotypic features characteristic of Down syndrome. We used FISH on metaphase chromosomes from translocation T65Dn/+ heterozygotes and Ts65Dn mice to show that the Chr 17 breakpoint is distal to the heterochromatin of Chr 17, that the Ts65Dn marker chromosome contains a small portion of Chr 17 euchromatin, that the Chr 16 breakpoint lies between the Ncam2 and Gabpa/App genes, and that the Ts65Dn chromosome contains >80% of the human Chr 21 homologs. The significance of this finding is discussed in terms of the utility of this mouse model.

Animal Diseases↗
PubMed2000

The sequence of human chromosome 21 and implications for research into Down syndrome.

The recent completion of the DNA sequence of human chromosome 21 has provided the first look at the 225 genes that are candidates for involvement in Down syndrome (trisomy 21). A broad functional classification of these genes, their expression data and evolutionary conservation, and comparison with the gene content of the major mouse models of Down syndrome, suggest how the chromosome sequence may help in understanding the complex Down syndrome phenotype.

Animals↗
PubMed2000

Transcription factor GATA-2 gene is located near 3q21 breakpoints in myeloid leukemia.

Rearrangements affecting chromosome band 3q21 are observed in a subgroup of patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). However, little is known about the molecular consequences of such aberrations. We therefore established a PAC contig in the 3q21 breakpoint region and identified potential protein coding sequences by exon trapping. One of the exons isolated was from the human GATA-2 gene, which we showed to be transcribed from telomere to centromere. The majority of 3q21 breakpoints are located telomeric to the transcribed portion of this gene in a region that in mice appears to be necessary for proper promoter function. Results of GATA-2 expression analyses in leukemic cell lines as well as primary patient samples are compatible with the hypothesis that 3q21 aberrations contribute to leukemogenesis through deregulation of the hematopoietic transcription factor GATA-2.

Acute Disease↗