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Biomedical subjects

F Gibson

Publications and source records attributed to F Gibson.

At least 37 records · Page 2Linked to original sources
PubMed2000

The clinical nurse specialist: perceptions of practising CNSs of their role and development needs.

This study was carried out to determine the role and development needs of Clinical Nurse Specialists (CNSs) in two acute hospital trusts. One of the aims was to obtain a detailed understanding of the current professional experience of Clinical Nurse Specialists. Data were collected using focus groups and analysed descriptively. Analysis of the content was qualitative, based on a grounded theory approach, and followed the initial steps of open and axial coding. Role transition and development needs are identified on a continuum of novice to expert.

Acute Disease↗
PubMed2000

The development of clinical competencies for use on a paediatric oncology nursing course using a nominal group technique.

This paper outlines the development of a competency model to be used to assess clinical competence during a post-registration specialist course. A nominal group technique was used to gather data about the detailed practice of paediatric oncology nurses. The nominal group technique was chosen to achieve consultation and consensus with a professional group. The six steps from undertaking the nominal group technique to implementation are described in detail. Some reflections on the use of competency statements are offered.

Child↗
PubMed2000

Establishing nursing research priorities on a paediatric haematology, oncology, immunology and infectious diseases unit: a Delphi survey.

For research to be successfully integrated and applied to practice, ownership and identification must come from those who are most likely to implement research into practice. This was one of the reasons for undertaking a Delphi survey to identify and rank the research priorities for clinical nursing research in a paediatric haematology, oncology, immunology and infectious diseases unit. The 'Nurses' Research Group' initiated the survey as a first step towards developing a strategy for evidence-based nursing. Four members of the research group volunteered to establish a working party to undertake the survey. This paper describes a four-round Delphi survey. The survey questionnaire was sent to all nursing staff on the unit. The initial process identified 151 research topics/themes. Through a process of refinement the priority list was reduced to 89. Repeat rounds were completed, culminating in the identification of four top priority areas of: symptom management, negotiation of care between the child and family, quality-of-life issues and retention of staff. The findings indicate directions for future clinical nursing research that will benefit specialist nurses, children and young people and their families. This paper provides a detailed account of the method, procedure and outcomes of the Delphi survey. The limitations of the Delphi survey method are also addressed and in this survey these included time (the length of time it took to complete the survey and time needed to complete each questionnaire), maintaining motivation of respondents, and the influence of researchers working in the research setting.

Journal Article↗
PubMed1999

Regions of variant histone His2AvD required for Drosophila development.

One way in which a distinct chromosomal domain could be established to carry out a specialized function is by the localized incorporation of specific histone variants into nucleosomes. H2AZ, one such variant of the histone protein H2A, is required for the survival of Drosophila melanogaster, Tetrahymena thermophila and mice (R. Faast et al., in preparation). To search for the unique features of Drosophila H2AZ (His2AvD, also referred to as H2AvD) that are required for its essential function, we have performed amino-acid swap experiments in which residues unique to Drosophila His2AvD were replaced with equivalently positioned Drosophila H2A.1 residues. Mutated His2AvD genes encoding modified versions of this histone were transformed into Drosophila and tested for their ability to rescue null-mutant lethality. We show that the unique feature of His2AvD does not reside in its histone fold but in its carboxy-terminal domain. This C-terminal region maps to a short alpha-helix in H2A that is buried deep inside the nucleosome core.

Amino Acid Sequence↗
PubMed1997

Mutation analysis of the mouse myosin VIIA deafness gene.

The shaker-1 (Myo7a) mouse deafness locus is encoded by an unconventional myosin gene: myosin VIIA [Gibson, Walsh, Mburu, Varela, Brown, Antonio, Biesel, Steel and Brown (1995) Nature (London) 374, 62-64]. The myosin VIIA gene is expressed in hair cells in the cochlea, where it is thought to function in the development of the critical neuroepithelium where auditory transduction takes place. In order to understand better the function of myosin VIIA, we have determined the complete sequence of the mouse myosin VIIA cDNA and employed the wild-type sequence for mutational analysis of a number of shaker-1 alleles. Analysis of the mouse myosin VIIA tail sequence demonstrates a large internal repeat with regions of similarity to myosins IV, X and XII as well as members of the band 4.1 family. In addition, the myosin VIIA repeats are similar along their entire length to a tail domain from a plant kinesin. The mouse myosin VIIA tail also contains a putative Src homology 3 (SH3) domain. Along with three previously reported shaker-1 mutations, mutations for seven shaker-1 alleles in total have now been identified. The mutational changes have been analysed in terms of their predicted effect on both myosin motor head and tail domain function and the predictions related to the known phenotypes of the shaker-1 alleles. Five of the mutations lie in the motor head, and analysis of their likely effect on myosin head structure correlates well with the known severity of the shaker-1 alleles. Of the two mutations in the tail, one is a missense mutation within the kinesin and myosin IV, X and XII homology domains that substitutes a conserved amino acid and leads to a severe deafness phenotype. This and other data suggest that myosin VIIA may have properties of a myosin-motor-kinesin-tail hybrid and be involved in membrane turnover within the actin-rich environment of the apical hair cell surface.

Amino Acid Sequence↗
PubMed1997

Unravelling the genetics of deafness.

Hearing-impaired mouse mutants not only are good models for human hereditary deafness, but also are extremely useful for understanding the molecular basis of the cochlear defect. We describe here how we identified the gene responsible for the deafness and vestibular defects in the shaker-1 mouse mutant as a myosin VII gene. Three different mutations, all causing the same phenotype in different lines of mouse, were found, providing good evidence that we had, indeed, found the correct gene. The same gene was subsequently found to be involved in Usher's syndrome type 1B, which features deafness, vestibular dysfunction, and progressive retinitis pigmentosa. The myosin VII gene is expressed in sensory hair cells, but not in supporting cells or neurons. We are investigating the role of myosin VII in hair cell development and function. Analysis of the different mutant stocks suggests it has at least two functions. First it is involved in the development and maintenance of the stereocilia bundle. Second, it has a role in inner hair cell function. No evidence of retinal degeneration like that in Usher's syndrome has been found in the shaker-1 mutants so far studied. The benefits of understanding the function of the gene for families with Usher's type 1B are discussed. This gene is the first to be identified as causing the most common type of disorder in human hearing impairment, neuroepithelial abnormalities, and suggests a new class of candidate genes for involvement in such defects.

Animals↗
PubMed1996

The coupling of the relative movement of the a and c subunits of the F0 to the conformational changes in the F1-ATPase.

F0F1-ATPase structural information gained from X-ray crystallography and electron microscopy has activated interest in a rotational mechanism for the F0F1-ATPase. Because of the subunit stoichiometry and the involvement of both a- and c-subunits in the mechanism of proton movement, it is argued that relative movement must occur between the subunits. Various options for the arrangement and structure of the subunits involved are discussed and a mechanism proposed.

Biological Transport↗
PubMed1995

Defective myosin VIIA gene responsible for Usher syndrome type 1B.

Usher syndrome represents the association of a hearing impairment with retinitis pigmentosa and is the most frequent cause of deaf-blindness in humans. It is inherited as an autosomal recessive trait which is clinically and genetically heterogeneous. Some patients show abnormal organization of microtubules in the axoneme of their photoreceptors cells (connecting cilium), nasal ciliar cells and sperm cells, as well as widespread degeneration of the organ of Corti. Usher syndrome type 1 (USH1) is characterized by a profound congenital sensorineural hearing loss, constant vestibular dysfunction and prepubertal onset of retinitis pigmentosa. Of three different genes responsible for USH1. USH1B maps to 11q13.5 (ref. 10) and accounts for about 75% of USH1 patients. The mouse deafness shaker-1 (sh1) mutation has been localized to the homologous murine region. Taking into account the cytoskeletal abnormalities in USH patients, the identification of a gene encoding an unconventional myosin as a candidate for shaker-1 (ref. 14) led us to consider the human homologue as a good candidate for the gene that is defective in USH1B. Here we present evidence that a gene encoding myosin VIIA is responsible for USH1B. Two different premature stop codons, a six-base-pair deletion and two different missense mutations were detected in five unrelated families. In one of these families, the mutations were identified in both alleles. These mutations, which are located at the amino-terminal end of the motor domain of the protein, are likely to result in the absence of a functional protein. Thus USH1B appears as a primary cytoskeletal protein defect. These results implicate the genes encoding other unconventional myosins and their interacting proteins as candidates for other genetic forms of Usher syndrome.

Adult↗
PubMed1995

A type VII myosin encoded by the mouse deafness gene shaker-1.

Genetic deafness is common, affecting about 1 in 2,000 births. Many of these show primary abnormalities of the sensory neuroepithelia of the inner ear, as do several hearing-impaired mouse mutants, suggesting that genes involved in sensory transduction could be affected. Here we report the identification of one such gene, the mouse shaker-1 (sh1) gene. Shaker-1 homozygotes show hyperactivity, head-tossing and circling due to vestibular dysfunction, together with typical neuroepithelial-type cochlear defects involving dysfunction and progressive degeneration of the organ of Corti. The sh1 gene encodes an unconventional myosin molecule of the type VII family. Three mutations are described, two mis-sense mutations and a splice acceptor site mutation, all in the region encoding the myosin head. The myosin type VII molecule encoded by sh1 is the first molecule to be identified that is known, by virtue of its mutations, to be involved in auditory transduction.

Amino Acid Sequence↗