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C Addison

Publications and source records attributed to C Addison.

36 records · Page 2Linked to original sources
PubMed1989

Cost-analysis of neonatal intensive and special care.

In the present economic climate and with increasing expenditure on neonatal intensive care, there has been a demand for economic evaluation and justification of neonatal intensive care programmes. This study assesses the inhospital costs of neonatal intensive care. Fixed and variable costs were calculated for services and uses of an Intensive/Special Care Nursery for the year 1985 and corrected to 1987 Australian dollar equivalents. Establishing a new neonatal intensive care unit of 43 costs in an existing hospital with available floor space including operating costs for a year were estimated in Australian dollars for 1987 at $6,408,000. Daily costs per baby for each were $1282 ventilator, $481 intensive, $293 transitional and $287 recovery, respectively. The cost per survivor managed in the Intensive/Special Care Nursery in 1985 showed the expected inverse relationship to birthweight being $2400 for greater than 2500 g, $4050 for 2000-2500 g, $9200 for 1500-1999 g, $23,900 for 1000-1499 g and $63,450 for less than 1000 g. Further analysis for extremely low birthweight infants managed in 1986 and 1987 demonstrated costs per survivor of $128,400 for infants less than 800 g birthweight and $43,950 for those 800-999 g. This methodology might serve as a basis for further accounting and cost-evaluation exercises.

Birth Weight↗
PubMed1988

The products of herpes simplex virus type 1 gene UL26 which are involved in DNA packaging are strongly associated with empty but not with full capsids.

We report on the properties of a family of related herpes simplex virus type 1 polypeptides (designated p40) of Mr around 40,000. The intracellular localization of these polypeptides has been examined using monoclonal antibodies and their association with viral capsids within the nuclei of infected cells has been demonstrated directly by immunoelectron microscopy. Specific DNA staining and the use of mutants defective for DNA packaging has revealed, in contrast to earlier findings, that p40 is present in empty capsids. Protein p40 is not present as a major component of full capsids or of mature virions indicating that it is transiently associated with capsids and that its removal from capsids is linked with the process of DNA packaging.

Capsid↗
PubMed1988

Two distinct regions of the murine p53 primary amino acid sequence are implicated in stable complex formation with simian virus 40 T antigen.

We mapped regions of the mouse p53 primary amino acid sequence implicated in stable complex formation with simian virus 40 T antigen. A number of mutant p53 proteins failed to complex stably with T antigen in vivo but formed stable complexes with T antigen in in vitro association assays. In contrast to an earlier report (T.-H. Tan, H. Wallis, and A. J. Levine, J. Virol. 59:574-583, 1986), our study showed that two distinct regions of p53 primary amino acid sequence, highly conserved between mouse and Xenopus laevis, were implicated in stable complex formation. Our data support the proposal that, when in complex, T antigen may occupy a site on p53 that is implicated in the normal function of the protein.

Amino Acid Sequence↗
PubMed1988

Characterization of mutant p53-hsp72/73 protein-protein complexes by transient expression in monkey COS cells.

Several mutant, but not wild-type, p53 proteins form complexes with hsp72/73 heat shock-related proteins in simian virus 40-transformed monkey COS cells. We carried out a detailed biochemical and structural mapping analysis of p53 and report here that p53-hsp72/73 complex formation showed considerable structural specificity. Such complexes were remarkably stable, but unlike analogous complexes formed between p53 and simian virus 40 T antigen, they did not form in in vitro association assays. p53-hsp72/73 complex formation in vivo appears to be dependent on aspects of mutant p53 protein conformation. However, absence of the conformation-sensitive epitope recognized by monoclonal antibody PAb 246 was not reliably diagnostic of such complexes, nor was p53-hsp72173 binding reliably diagnostic of oncogenic activation.

Animals↗
PubMed1988

Mouse p53 blocks SV40 DNA replication in vitro and downregulates T antigen DNA helicase activity.

Immunopurified mouse p53 proteins were used to gain experimental access to the mechanisms underlying nonprimate p53 directed suppression of SV40 origin directed DNA replication in vivo. In replication competent HeLa cell extracts containing exogenous T antigen, mouse p53 blocks T antigen dependent DNA synthesis as in vivo. However, in transcription competent HeLa extracts, mouse p53 has no effect either on overall transcription or on the ability of immunopurified T antigen to downregulate SV40 early transcription. We show that although mouse p53 has no significant effect on T antigen encoded activities such as ATPase and DNA binding, helicase activity is somewhat reduced suggesting that the in vivo suppression by mouse p53 of SV40 replication may be due, at least in part, to direct modulation of T antigen function.

Adenosine Triphosphatases↗
PubMed1984

Characterisation of a herpes simplex virus type 1 mutant which has a temperature-sensitive defect in penetration of cells and assembly of capsids.

A herpes simplex virus type 1 (HSV-1) mutant, ts1204, which has a temperature-sensitive (ts) mutation located within genome map coordinates 0.318 to 0.324, close to but outside the coding sequences of the glycoprotein gB gene, has been characterised. Although this mutant adsorbed to the cell surface at the nonpermissive temperature (NPT), it failed to penetrate the cell membrane. As a consequence of this defect, high multiplicities of infection of ts1204 blocked subsequent infection of cells by wild-type HSV-1. By contrast, at the NPT, superinfection of cells with HSV-2 was not inhibited by prior infection with ts1204. The penetration defect could be overcome either by brief incubation of mutant virus-infected cells at the permissive temperature, or by treatment of the cells with polyethylene glycol, a compound which promotes fusion of membranes. Upon continued incubation of ts1204-infected cells at the NPT, low numbers of capsids were assembled. Although these capsids all had some internal structure, they did not contain DNA. Another mutant, ts1208, which lies in the same complementation group as ts1204, penetrated cells normally at the NPT, but like ts1204, had a defect in the formation of functional capsids. Evidence presented in this paper suggests that the gene in which the ts1204 and ts1208 lesions map encodes a structural polypeptide.

Animals↗
PubMed1983

In vivo and in vitro hamster models in the assessment of virulence of recombinant influenza viruses.

The virulence of five wild-type influenza A viruses and 14 recombinant viruses, prepared from the cold adapted A/Ann Arbor/6/60 virus and various wild-type viruses, was studied by two methods. Firstly, the viruses were inoculated into hamsters, and the titres present in the lungs and turbinates at 1, 3 and 4 days post-infection were measured. Secondly, the effect of five wild-type and ten recombinant viruses on the ciliated epithelium of in vitro hamster tracheal organ cultures was examined. The results obtained were assessed with reference to the known virulence of the viruses for human volunteers. The results showed that virus strains virulent for man grew to higher titres in hamster lungs and turbinates than attenuated strains; and that virulent strains destroyed the ciliary activity of hamster tracheal organ cultures more quickly and to a greater extent than attenuated strains. Comparison of the results with the known virulence of viruses tested for man suggests that the reduced ability of virus to grow in hamster lung tissue and the relatively little effect on ciliary activity may be used as markers of virus attenuation; however, the growth of virus in hamster turbinates overlaps for virulent and attenuated strains and therefore was not considered a useful marker of virulence.

Animals↗
PubMedDate not supplied

Mouse p53 inhibits SV40 origin-dependent DNA replication.

p53 is a cellular phosphoprotein that is present at elevated concentrations in cells transformed by different agents. p53 complementary DNA expression-constructs immortalize primary cells in vitro and co-operate with an activated ras oncogene in malignant transformation. Several reports have implicated p53 in mammalian cell cycle control and specifically with events occurring at the G0-G1 boundary. p53 forms specific complexes with simian virus 40 (SV40) large-T antigen, and such complexes are found associated with both replicating and mature SV40 DNA in lytically infected cells. In an accompanying paper Gannon and Lane report that in in vitro plate-binding assays, mouse p53 can displace polymerase alpha from complex with T-antigen. We have examined the in vivo consequences of expressing wild-type and mutant p53 proteins from other species in SV40-transformed monkey cells. We report here that expression of mouse p53 results in a substantial and selective inhibition of SV40 origin-dependent DNA replication. In addition to any function in the G0-G1 transition, the data presented suggest that p53 may affect directly the initiation or maintenance of replicative DNA synthesis.

Animals↗
PubMedDate not supplied

Benchmarking best practice for external ventricular drainage.

Sharing of best practice and use of all available evidence is important in developing effective clinical guidelines for nursing practice. This can be achieved through benchmarking. Sharing of good practice and achieving consensus guidelines can avoid repetition of effort by nurses engaged in similar fields of practice. The Pan London Neuroscience Practice Development Forum was established in 1998 to share best practice within the field of neuroscience nursing across London. The Pan London Forum has now achieved consensus and developed evidence-based clinical guidelines for the management of external ventricular drainage. Within the scope of this article, the principles of external ventricular drainage will be highlighted, before identifying the evidence base for nursing management of patients. Approaches for troubleshooting common problems will also be discussed and the benchmarked clinical guidelines will be presented.

Benchmarking↗
PubMedDate not supplied

Self-medication for elderly patients.

This paper describes the introduction of a self-medication programme for elderly in-patients using action research. The programme was initiated by a steering group which met regularly to implement and monitor self-medication. Ward staff were interviewed to assess their learning needs before the start, meetings were held as the project advanced, and a final staff evaluation questionnaire was administered. Patients' opinions were also monitored. Self-medication was successfully introduced and minor problems were rapidly solved by participating staff. Patients were highly satisfied with the new independence and self-esteem they had gained through taking their own medications. Nurses shared these feelings, but also felt that self-medication was more time consuming than previous drug rounds. Suggestions for further research and development are given.

Aged↗