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R Fulton

Publications and source records attributed to R Fulton.

At least 19 recordsLinked to original sources
PubMed2000

Content-based retrieval of dynamic PET functional images.

The recent information explosion has led to massively increased demand for multimedia data storage in integrated database systems. Content-based retrieval is an important alternative and complement to traditional keyword-based searching for multimedia data and can greatly enhance information management. However, current content-based image retrieval techniques have some deficiencies when applied in the biomedical functional imaging domain. In this paper, we presented a prototype design for a content-based functional image retrieval database system for dynamic positron emission tomography. The system supports efficient content-based retrieval based on physiological kinetic features and reduces image storage requirements. This design makes it possible to maintain a large number of patient data sets online and to rapidly retrieve dynamic functional image sequences for interpretation and generation of physiological parametric images, and offers potential advantages in medical image data management and telemedicine, as well as providing possible opportunities in the statistical and comparative analysis of functional image data.

Computer Graphics↗
PubMed1999

The fit-1 common integration locus in human and mouse is closely linked to MYB.

The fit-1 locus was originally identified as a common insertion site for feline leukemia virus (FeLV) in thymic lymphosarcomas induced by FeLV-myc recombinant viruses, suggesting that it harbors a gene that cooperates with Myc in T-cell leukemogenesis. We have previously mapped the fit-1 locus to feline Chromosome (Chr) B2. We have now identified conserved sequences that allow the mapping of the murine homolog using the European Interspecific Backcross (EUCIB). This shows that fit-1 is located on mouse Chr 10, 1cM proximal to Ahi-1, a murine retroviral integration locus that is closely linked to Myb. Moreover, the physical linkage to MYB is maintained in the human genome, as shown by cloning of the human homolog of fit-1 from a Chr 6 cosmid library and a series of overlapping PAC clones. Generation of a contig map around the human homolog of fit-1 reveals that it is approximately 100-kb upstream of MYB. In addition to fit-1 and Ahi-1, two other common insertion sites, Mis-2 and Mml-1, have also been mapped adjacent to Myb on mouse Chr 10. Previous analysis of tumors carrying insertions at fit-1, Mml-1, Mis-2 and Ahi-1 showed no obvious abnormalities in Myb expression. However, the cluster of viral insertion loci in this region suggests either the presence of a closely linked activation target or that subtle effects on Myb have been overlooked.

Animals↗
PubMed1999

Nucleotide sequence of the feline Bmi-1 coding region.

The bmi-1 gene was discovered as a clonal integration site of the Moloney murine leukaemia virus in B-cell lymphomas. The Bmi-1 protein contains the RING finger motif and is homologous to two Drosophila proteins known to be part of a multimeric protein complex involved in repressing gene transcription. A similar role for the highly conserved Bmi-1 protein in mammalian cells has been suggested. The coding regions for the mouse and human genes are known and are 92% homologous. This study involved PCR amplification, cloning, and sequencing of the 980bp feline bmi-1 coding region which was shown to be 92% and 97% homologous to the mouse and human genes respectively. From the open reading frame the feline protein is 326 amino acids in length and is 99% homologous to the human protein and 97% homologous to the mouse protein. This data is consistent with the closer relationship between the feline and human genomes and provides another experimental system in which to analyse Bmi-1 function.

Amino Acid Sequence↗
PubMed1996

Octamer independent activation of transcription from the kappa immunoglobulin germline promoter.

Previous analyses of immunoglobulin V region promoters has led to the discovery of a common octamer motif which is functionally important in the tissue-specific and developmentally regulated transcriptional activation of immunoglobulin genes. The germline promoters (Ko) located upstream of the J region gene segments of the kappa locus also contain an octamer motif (containing a single base pair mutation and referred to as the variant octamer) which has been shown previously to bind Oct-1 and Oct-2 transcription factors in vitro. To further elucidate the role of this variant octamer motif in the regulation of germline transcription from the unrearranged kappa locus, we have quantitated the relative binding affinity of Oct-1 and Oct-2 for the variant octamer motif and determined the functional role of this octamer motif in transcriptional activation. We find that, although the variant octamer motif binds Oct-1 and Oct-2 in vitro with 5-fold lower affinity than the consensus octamer motif, mutation of the variant octamer motif to either a consensus octamer or non-octamer motif has no effect on transcriptional activation from the germline promoter. We also find significant differences in activation of germline and V region promoters by kappa enhancers. Our results suggest that the germline promoters and V region promoters differ in their dependence on octamer for activation and respond differently to enhancer activation. These findings have important implications in regulation of germline transcription as well as concomitant activation of the V-J recombination of the kappa light chain locus.

Animals↗
PubMed1996

Multiple phenotypes associated with Myc-induced transformation of chick embryo fibroblasts can be dissociated by a basic region mutation.

Chimaeric alleles were constructed to assay the biological functions of an N-terminal deletion and C-terminal mutations which were found in a naturally occurring mutant of feline vMyc, T17. The mutant alleles were assayed for their ability to transform chick embryo fibroblasts in vitro by a number of criteria, namely the ability to induce morphological transformation, an accelerated growth rate and growth in soft agar. Feline cMyc could transform the avian cells, whilst T17 vMyc could not, and the N-terminal deletion was responsible for conferring the primary transformation defect on the mutant protein. The C-terminal mutations which consist of a point mutation adjacent to the nuclear localisation signal and a point mutation/amino acid insertion within the basic region (BR) could, however, dissociate the Myc-induced parameters of transformation. This effect was a specific function of the BR mutation alone, and the mutation could be transferred into avian cMyc with comparable biological consequences. The BR mutation did not disrupt the sequence specific DNA binding activity of the protein in vivo, despite exerting a biological effect. These data suggest a novel phenotype where the mutation may affect a subset of Myc-regulated genes through altered DNA binding specificity or protein-protein interactions.

Amino Acid Sequence↗
PubMed1996

Allogeneic marrow transplantation in a cat with acute myeloid leukemia.

A listless, anorectic 2-year-old cat was found to have a normocytic, nonregenerative anemia. A diagnosis of acute myeloid leukemia type M6Er was made. Because the cat was young, had negative FeLV and feline immunodeficiency virus test results, had a sibling that could be used as a bone marrow donor, had received only 1 transfusion, and was in good health other than being anemic, allogeneic bone marrow transplantation (BMT) was attempted using marrow from the cat's sibling. The most life-threatening complication following BMT was hemorrhage caused by severe thrombocytopenia. Complete hematopoietic engraftment was evident 36 days after BMT. The cat then was discharged to its owner. In the first year, the cat continued to improve with the exception of an intractable dermatophytosis, which resolved eventually. The cat continues to do well 4 years after BMT. To our knowledge, this represents the first report of successful allogeneic BMT for a cat with acute myeloid leukemia.

Anemia↗
PubMed1996

Apparent uncoupling of oncogenicity from fibroblast transformation and apoptosis in a mutant myc gene transduced by feline leukemia virus.

The T17 v-myc oncogene was transduced by feline leukemia virus in a spontaneous feline T-cell lymphosarcoma. Molecular cloning and sequencing of the v-myc gene revealed several unique mutations, including a large deletion affecting amino acids 49 to 124 and a 3-bp insertion within the basic DNA binding domain which converts Leu-362 to Phe-Arg. The T17 lymphoma cell line was found to express a truncated 50-kDa Myc protein at exceptionally high levels, while the endogenous c-myc gene was not detectably expressed. These observations suggest that the mutant Myc product expresses an oncogenic function in T cells. Further evidence that the T17 mutant gene retains oncogenic potential was provided by its detection in clonally integrated proviruses in secondary tumors induced by feline leukemia virus T17, where no reversion mutations were found in any of three tumors examined. However, the mutant T17 v-myc gene did not induce transformation in a chicken embryo fibroblast assay, in contrast to wild-type feline c-myc, which conferred higher growth rates on the chicken fibroblasts, along with altered morphology and the ability to form foci in soft agar. Chicken cells over-expressing feline c-myc died by apoptosis when cultured with low serum concentrations, while the T17 mutant had no discernible effect. These results suggest that the leukemogenic potential of Myc can be uncoupled from its ability to cause transformation in fibroblasts. A possible explanation for this apparent paradox is that developing T cells are acutely sensitive to a subset of Myc functions which are insufficient for fibroblast transformation.

Amino Acid Sequence↗