Biomedical subjects
Publications and source records attributed to F Gibson.
The alteration of blood flow in the skin and subcutaneous tissue due to mechanical loading is of great importance in the prevention of decubitus ulcers. A technique is described for assessing changes in blood content optically. The results indicate that such changes occur after loading even though the deformation is maintained constant.
The aim of the study was to establish current UK oral care practice for children with cancer. A telephone survey of all 22 United Kingdom Children's Cancer Study Group (UKCCSG) centres was undertaken. Nineteen (86%) of the centres reported using guidelines/protocols for mouth care. The use of routine preventive oral care therapies showed the greatest variation between centres. Four centres (18%) did not use any prophylactic oral care therapy other than basic oral hygiene, whereas seven (32%) routinely used a combination of three or more agents. Chlorhexidine was the most frequently administered prophylactic therapy (17/22 centres, 77%), followed by nystatin (11/22 centres, 50%). There was little variation in advice given to parents/patients on basic oral hygiene. Regarding dental check-ups, 9/22 centres (41%) recommended children to attend a hospital-linked dental clinic. Only at 8/22 centres (36%) did children undergo a dental check-up before commencing cancer treatment. The survey identified significant variation in preventive oral care therapies and dental check-ups at the UKCCSG centres. Attention needs to be given to establishing evidence based, effective strategies.
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Although fatigue has been a focus for research in adult cancer care for some time, the same cannot be said for adolescent oncology practice. This paper summarises the literature concerning fatigue in adolescents with, and following, cancer diagnoses, drawing on data from four empirical studies. Fatigue is multidimensional, multifactorial and highly subjective, but can be managed to enhance self-caring and coping strategies. All of the studies reviewed within indicate that fatigue is a troublesome symptom, which impacts on quality of life. From this review, we set up a research study. This paper provides a brief report of preliminary data from this study drawn from a group of adolescents in late remission from childhood cancer. These data are used to evaluate the utility of focus groups as a method of data collection in exploring the concept of fatigue in adolescents. Concurring with the studies we reviewed, findings from the preliminary data suggest that fatigue is a highly subjective and 'abnormal' phenomenon that holds a variety of implied meanings and associated metaphors connected with past experiences of childhood cancer. The focus group proved to be a viable research method to facilitate mutual disclosure and provoke discussion. Recognition of the research challenges with adolescents, where there is the potential for a range of meanings for the experience of fatigue, is an important finding for future studies.
Monocyte chemoattractant protein 1 (MCP-1) is an important chemokine that induces monocyte recruitment in a number of different pathologies, including infection. To investigate the role of MCP-1 in protecting a host from a chronic interstitial polymicrobial infection, dental pulps of MCP-1(-/-) mice and controls were inoculated with six different oral pathogens. In this model the recruitment of leukocytes and the impact of a genetic deletion on the susceptibility to infection can be accurately assessed by measuring the progression of soft tissue necrosis and osteolytic lesion formation. The absence of MCP-1 significantly impaired the recruitment of monocytes, which at later time points was threefold higher in the wild-type mice than in MCP-1(-/-) mice (P < 0.05). The consequence was significantly enhanced rates of soft tissue necrosis and bone resorption (P < 0.05). We also determined that the MCP-1(-/-) mice were able to recruit polymorphonuclear leukocytes (PMNs) to a similar or greater extent as controls and to produce equivalent levels of Porphyromonas gingivalis-specific total immunoglobulin G (IgG) and IgG1. These results point to the importance of MCP-1 expression and monocyte recruitment in antibacterial defense and demonstrate that antibacterial defense is not due to an indirect effect on PMN recruitment or modulation of the adaptive immune response.
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This paper provides an overview of the EONS (European Oncology Nursing Study) core curriculum revision project. The aim of this project was to revise the EONS core curriculum for a Post-Basic Course in Cancer Nursing, first published in 1989, so that it would better reflect patient and family need and contemporary cancer nursing practice. A further aim of the project was to address the educational needs of both adult and paediatric oncology nurses. To achieve these aims a core curriculum revision meeting was organized and attended by representatives from most of the EU Member States. A rough draft of the core curriculum was developed, circulated and subjected to further scrutiny and modification. Following approval of the final draft, the core curriculum was translated from English into the 10 other official EU languages and made available in both paper and electronic form. The updated core curriculum was launched during the ECCO-10 conference and has now been disseminated widely amongst European cancer nurses and the wider nursing and medical community.
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The concurrent use of an oral assessment guide and oral care algorithm proved valuable in providing a more consistent approach to the oral care of children on a particular paediatric oncology ward (Gibson et al. 1997). However, as action research was chosen to develop practice, the diagnosis of new problems was anticipated. The identification of problem areas arose from two sources-informal feedback from the practice setting and via a formal audit using a tripartite approach consisting of a structured interview, vignettes and an analysis of existing documentation. The findings firstly demonstrated that practitioners experienced problems associated with the interpretation of the information contained within the existing algorithm. Secondly, there was also strong evidence to show that the production of a second 'therapeutic' algorithm would be beneficial to patient care. Finally, to ensure clarity, minor changes were required to the oral assessment guide. By using a collaborative approach between researchers and practitioners a positive resolution to a commonly identified clinical problem was expedited.
OBJECTIVE: Bone mineral density (BMD) in later life is a major determinant of osteoporotic fracture risk and has been shown to be under strong genetic influence. Transforming growth factor beta 1 (TGF-beta 1) is an important regulatory cytokine, is found in high concentrations in the bone matrix, and is a plausible candidate for the genetic regulation of BMD. METHODS: This study investigated whether a novel polymorphism within the TGF-beta 1 gene is associated with BMD in a large normal female population of 1706 dizygotic (DZ) twins (age range 18-76 yr). RESULTS: A C--->T [corrected] polymorphism was identified in intron 5, the T [corrected] allele having a frequency of 0.25. Subjects homozygous for the presence of the TGF-beta 1 T [corrected] allele had a 4% reduction in femoral neck BMD compared with the other two genotype groups (P<0.025). No effect was seen at the lumbar spine or ultradistal radius, or with calcaneal ultrasound measurements. Results were unaffected after adjustment for potential confounders. These findings were predominantly seen in pre-menopausal subjects, suggesting that this locus has an effect on the attainment of peak BMD. In pre-menopausal women, subjects who were homozygous for the T [corrected] allele had a 5-fold excess risk of having osteoporosis at the femoral neck compared with the other genotype groups. A within-pair analysis using the sibling transmission disequilibrium test confirmed these findings in pre-menopausal women and supported the candidacy of the TGF-beta 1 locus in the genetic regulation of hip BMD. CONCLUSIONS: These results indicate that allelic variation at the TGF-beta 1 gene contributes to the development of osteoporosis at the hip. The study also highlights the power of candidate gene analysis in twins, in whom loci having modest effects on disease risk can be identified.
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This paper reports on the use of focus groups to investigate the development of clinical nurse specialist roles. The need for this project was identified during initial research, undertaken in two London Hospital Trusts, to assess the variety and nature of advanced clinical nursing roles already in evidence. From analysis of these data, this second stage of the research developed, in which the future of the clinical nurse specialist role within these two trust settings was explored. The initial steps of grounded theory, analytical techniques and procedures, using a constant comparative method, were used to analyse the findings from five focus groups (composed of a total of 25 nurses from two trusts). From the data, six categories were identified; role components; experience versus education; supportive strategies; personal qualities; future role development and development strategies. These categories provide the framework for discussing the findings of the research, within the context of the available literature. This examination of the clinical nurse specialist role highlights issues for career progression and education strategies. Both will need careful planning, in order for the clinical nurse specialist role to be considered and evolve as part of a potential strategy for the development of nursing roles within the two trusts and on a national level.
The solution structures of three related peptides (A1, A2, and A9) corresponding to the Thr(671)-Leu(690) region of the skeletal muscle dihydropyridine receptor II-III loop have been investigated using nuclear magnetic resonance spectroscopy. Peptide A1, the native sequence, is less effective in activating ryanodine receptor calcium release channels than A2 (Ser(687) to Ala substitution). Peptide A9, Arg(681)-Ser(687), does not activate ryanodine receptors. A1 and A2 are helical from their N terminus to Lys(685) but are generally unstructured from Lys(685) to the C terminus. The basic residues Arg(681)-Lys(685), essential for A1 activation of ryanodine receptors, are located at the C-terminal end of the alpha-helix. Peptide A9 was found to be unstructured. Differences between A1 and A2 were observed in the C-terminal end of the helix (residues 681-685), which was less ordered in A1, and in the C-terminal region of the peptide, which exhibited greater flexibility in A1. Predicted low energy models suggest that an electrostatic interaction between the hydroxyl oxygen of Ser(687) and the guanidino moiety of Arg(683) is lost with the Ser(687)Ala substitution. The results show that the more structured peptides are more effective in activating ryanodine receptors.
Characterisation of 35 Kluyveromyces lactis strains lacking mitochondrial DNA has shown that mutations suppressing rho(0)-lethality are limited to the ATP1, 2 and 3 genes coding for the alpha-, beta- and gamma- subunits of mitochondrial F(1)-ATPase. All atp mutations reduce growth on glucose and three alleles, atp1-2, 1-3 and atp3-1, produce a respiratory deficient phenotype that indicates a drop in efficiency of the F(1)F(0)-ATP synthase complex. ATPase activity is needed for suppression as a double mutant containing an atp allele, together with a mutation abolishing catalytic activity, does not suppress rho(0)-lethality. Positioning of the seven amino acids subject to mutation on the bovine F(1)-ATPase structure shows that two residues are found in a membrane proximal region while five amino acids occur at a region suggested to be a molecular bearing. The intriguing juxtaposition of mutable amino acids to other residues subject to change suggests that mutations affect subunit interactions and alter the properties of F(1) in a manner yet to be determined. An explanation for suppressor activity of atp mutations is discussed in the context of a possible role for F(1)-ATPase in the maintenance of mitochondrial inner membrane potential.
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