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Biomedical subjects

D Hewett

Publications and source records attributed to D Hewett.

12 recordsLinked to original sources
PubMed2000

Postal consent for upper gastrointestinal endoscopy.

BACKGROUND: Standards for good practice in clinical risk management issued by the Clinical Negligence Scheme for Trusts indicate that "appropriate information is provided to patients on the risks and benefits of proposed treatment, and of the alternatives available before a signature on a consent form is sought". AIMS: To investigate the practicability and patient acceptability of a postal information and consent booklet for patients undergoing outpatient gastroscopy. METHODS: Information about gastroscopy procedure, personalised appointment details, and a carbonised consent form were compiled into a single booklet. This was mailed to patients well in advance of their endoscopic procedure. Patient satisfaction for this new process was assessed by questionnaire. RESULTS: 275 patients received a patient information booklet. Of these, 150 (54.5%) returned the consent form by post when they confirmed their attendance; 141 (94%) had signed the form, and the other nine requested further information. Of the remaining 125 booklets sent out, 115 (92%) forms were brought back on the day of the investigation having been previously signed. The remaining 10 (8%) required further information before signing the form. An audit of 168 patients was used to test reaction to the booklet and the idea of filling in the form before coming to hospital; 155 patients (92. 2%) reported the information given in the booklet to be "very useful", and all reported it to be "clear and understandable". CONCLUSION: A specifically designed patient information booklet with integral consent form is accepted by patients, and improves the level of understanding prior to the investigation being carried out.

Appointments and Schedules↗
PubMed1997

Human chromosomal fragile site FRA16B is an amplified AT-rich minisatellite repeat.

Fragile sites are nonstaining gaps in chromosomes induced by specific tissue culture conditions. They vary both in population frequency and in the culture conditions required for induction. Folate-sensitive fragile sites are due to expansion of p(CCG)n trinucleotide repeats; however, the relationship between sequence composition and the chemistry of induction of fragile sites is unclear. To clarify this relationship, the distamycin A-sensitive fragile site FRA16B was isolated by positional cloning and found to be an expanded 33 bp AT-rich minisatellite repeat, p(ATATA TTATATATTATATCTAATAATATATC/ATA)n (consistent with DNA sequence binding preferences of chemicals that induce its cytogenetic expression). Therefore the mutation mechanism associated with trinucleotide repeats is also a property of minisatellite repeats (variable number tandem repeats).

Base Composition↗
PubMed1997

Genetic heterogeneity in familial acute myelogenous leukemia: evidence for a second locus at chromosome 16q21-23.2.

The identification of genes responsible for the rare cases of familial leukemia may afford insight into the mechanism underlying the more common sporadic occurrences. Here we test a single family with 11 relevant meioses transmitting autosomal dominant acute myelogenous leukemia (AML) and myelodysplasia for linkage to three potential candidate loci. In a different family with inherited AML, linkage to chromosome 21q22.1-22.2 was recently reported; we exclude linkage to 21q22.1-22.2, demonstrating that familial AML is a heterogeneous disease. After reviewing familial leukemia and observing anticipation in the form of a declining age of onset with each generation, we had proposed 9p21-22 and 16q22 as additional candidate loci. Whereas linkage to 9p21-22 can be excluded, the finding of a maximum two-point LOD score of 2.82 with the microsatellite marker D16S522 at a recombination fraction theta = 0 provides evidence supporting linkage to 16q22. Haplotype analysis reveals a 23.5-cM (17.9-Mb) commonly inherited region among all affected family members extending from D16S451 to D16S289. In order to extract maximum linkage information with missing individuals, incomplete informativeness with individual markers in this interval, and possible deviance from strict autosomal dominant inheritance, we performed nonparametric linkage analysis (NPL) and found a maximum NPL statistic corresponding to a P-value of .00098, close to the maximum conditional probability of linkage expected for a pedigree with this structure. Mutational analysis in this region specifically excludes expansion of the AT-rich minisatellite repeat FRA16B fragile site and the CAG trinucleotide repeat in the E2F-4 transcription factor. The "repeat expansion detection" method, capable of detecting dynamic mutation associated with anticipation, more generally excludes large CAG repeat expansion as a cause of leukemia in this family.

Chromosome Mapping↗
PubMed1994

Differential allelic expression of a fibrillin gene (FBN1) in patients with Marfan syndrome.

Marfan syndrome is a connective-tissue disorder affecting cardiovascular, skeletal, and ocular systems. The major Marfan locus has been identified as the FBN1 gene on chromosome 15; this codes for the extracellular-matrix protein fibrillin, a 350-kD constituent of the 8-10-nm elastin-associated microfibrils. We identified five MFS patients who were heterozygous for an RsaI restriction-site dimorphism in the 3' UTR of the FBN1 gene. This expressed variation was used to distinguish the mRNA output from each of the two FBN1 alleles in fibroblast cultures from these five patients. Three of the patients were shown to produce < 5% of the normal level of FBN1 transcripts from one of their alleles. This null-allele phenotype was not observed in 10 nonmarfanoid fibroblast cell lines.

Adult↗
PubMed1992

Genetic linkage of the Marfan syndrome, ectopia lentis, and congenital contractural arachnodactyly to the fibrillin genes on chromosomes 15 and 5. The International Marfan Syndrome Collaborative Study.

BACKGROUND: The large glycoprotein fibrillin is a structural component of elastin-containing microfibrils found in many tissues. The Marfan syndrome has been linked to the fibrillin gene on chromosome 15, but congenital contractural arachnodactyly, which shares some of the physical features of the syndrome, has been linked to the fibrillin gene on chromosome 5. METHODS: Using specific markers for the fibrillin genes, we performed genetic linkage analysis in 28 families with the Marfan syndrome and 8 families with four phenotypically related disorders--congenital contractural arachnodactyly (3 families), ectopia lentis (2), mitral-valve prolapse syndrome (2), and annuloaortic ectasia (1). RESULTS: Genetic linkage was established between the Marfan syndrome and only the fibrillin gene on chromosome 15, with a maximum lod score of 25.6 (odds for linkage, 10(25.6):1). Ectopia lentis was also linked to the fibrillin gene on chromosome 15, whereas congenital contractural arachnodactyly was linked to the fibrillin gene on chromosome 5. There was no linkage of mitral-valve prolapse to the fibrillin gene on chromosome 5; studies of chromosome 15 were not informative. Annuloaortic ectasia was not linked to either fibrillin gene. CONCLUSIONS: The Marfan syndrome appears to be caused by mutations in a single fibrillin gene on chromosome 15. Diagnosis of the Marfan syndrome by genetic linkage and analysis is now feasible in many families.

Base Sequence↗
PubMed1978

Designing a comprehensive service for a health care group: a framework for planning.

This article describes an exercise which was designed by a multidisciplinary group, including a community physician, health economist, clinician and operational research practitioner, to explore the essential nature of planning services for a particular health care group. The first programme, described in the article, was concerned with psychogeriatric services, including both community and hospital provision, but it is indicated that the exercise can be adapted to all other services, and has already been used to evolve a comprehensive accident and emergency service in a particular health area. Participants came from a wide variety of disciplines, including community medicine, psychiatry, geriatrics, hospital and community nursing and non-medical administration. The tutors to the course were those who had been involved in its planning and they spent the time working with the participants to explore the concepts involved and to produce some practical solutions that could be used in the field.

Decision Making↗
PubMed1978

A comparison of methods using diaminobenzidine (DAB) to localize peroxidases in erythrocytes, neutrophils, and peroxidase-antiperoxidase complex.

Reactions using diaminobenzidine (DAB) to localize the enzyme peroxidase in neutrophils and peroxidase-antiperoxidase (PAP) complex during immunological staining are usually performed in Tris-HCl or phosphate buffer at pH 7.2-7.6. However, DAB solutions at pH 7.2-7.6 often demonstrate erythrocyte pseudoperoxidase as well. By lowering the pH of the DAB solutions, it is possible to selectively suppress the reactivity of pseudoperoxidase while maintaining optimal reactions in neutrophils and PAP complex. For this purpose we recommend ammonium acetate-citric acid buffer at pH 5.5 (pH 5.0-6.0) containing 44 mg DAB per 100 ml buffer and 0.003%-0.03% with respect to H2O2.

3,3'-Diaminobenzidine↗
PubMedDate not supplied

Towards a model for hospital case-load decision support.

This paper presents an operational model of patient flow through a hospital. The operations involved in the patient flow are explained and the development and use of the model are discussed. The model uses the data derived from the NHS minimum contract data set which is collected by all hospitals, and this results in the model being generalizable to any hospital. Typically the model can be used to determine the appropriate bed numbers for a given arrival pattern, or the effects of particular management strategies or changes in patient care patterns on the hospital. The model is implemented on a PC running the Microsoft Windows operating environment, and solved used a simulation approach.

Bed Occupancy↗