Biomedical subjects
Publications and source records attributed to J Price.
Using a systems approach, critical pathways address different types of injuries in trauma patients. A 640-bed tertiary referral center contracted with an independent consultant to evaluate its trauma program, resulting in several improvements in the delivery of services. Case management achieved the action plan goals: improved utilization of resources, improved continuity of care, and decreased length of stay.
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PURPOSE: We describe a patient who presented with severe anemia and ectodermal dysplasia. PATIENTS AND METHODS: This is a case report of a patient whose anemia was evaluated at New York Hospital and then returned to Australia where further testing was performed. RESULTS: The history indicated that this was a chronic anemia. Bone marrow examination showed binucleated late normoblasts consistent with congenital dyserythropoietic anemia type II (CDA II) and not dyskeratosis congenita. Paroxysmal nocturnal hemoglobinuria was excluded despite the presence of a positive sucrose hemolysis test. Other types of acquired and congenital anemias were excluded by testing. CONCLUSIONS: This is the first patient reported with coincident CDA II and ectodermal dysplasia.
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We have studied the question of whether a retrovirus integrates into the chromosomal DNA of the host cell before or after the DNA is replicated during the S phase of the cell cycle. We have infected single NIH-3T3 cells with BAG, a replication-incompetent retroviral vector which encodes the lacZ gene, then observed the clones derived from these cells to discover whether all the cells carry a copy of the proviral DNA. We have discovered that only half of the progeny of an infected cell carries a copy of the provirus. This indicates that the virus only integrates into post-replication DNA. We discuss the implications of this result for applications of retroviruses, such as gene therapy and cell lineage, which use them as vehicles for gene transfer into stem cells.
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We have performed experiments which demonstrate that puromycin inhibits the import of proteins into mitochondria in in vitro reactions containing mitochondria isolated from the yeast Saccharomyces cerevisiae and precursor proteins synthesized in a nuclease-treated rabbit reticulocyte lysate. Puromycin inhibited the import of several precursor proteins including; a fusion protein consisting of the first 22 N-terminal residues of yeast cytochrome oxidase subunit IV fused to mouse dihydrofolate reductase, both a destabilized and truncated form of this same fusion protein, the beta-subunit of the yeast mitochondrial F1-ATPase and yeast alcohol dehydrogenase III. The insertion of the yeast outer mitochondrial protein porin was not inhibited by puromycin. Puromycin-induced import inhibition could be overcome by adding additional ATP to the import reactions. However, if access of ATP to the mitochondrial matrix was prevented by blocking the adenine nucleotide translocase with carboxyatractyloside, ATP addition was unable to overcome the inhibitory effect of puromycin on protein import. Collectively, these results demonstrate that puromycin inhibits protein import into mitochondria by interfering with an ATP-dependent step in the import process and that the ATP-dependent component in the reaction is located inside the inner mitochondrial membrane. In addition to supporting the view that ATP is required in the matrix for efficient protein import, these results may provide a useful tool for identifying the ATP-binding components of the import apparatus.
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Benzodiazepine receptor number and affinity were measured in vivo with single photon emission tomography (SPECT). Following an initial bolus injection, the radiotracer [123I]iomazenil was infused at a constant rate for 5 to 8 h. This procedure induced a state of sustained equilibrium at the receptor level. Nondisplaceable activity was measured after injection of a receptor saturating dose of flumazenil. Experiments performed at high and low specific activity permitted estimation of an equilibrium binding affinity constant of 0.47 nM and a maximum binding capacity of 127 nM in occipital cortex.
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Keratin 8 (mK8) and its partner keratin 18 (mK18) are the first intermediate filament proteins expressed during mouse embryogenesis. They are found in most extraembryonic and embryonic simple epithelia, including trophectoderm, visceral yolk sac, gastrointestinal tract, lungs, mammary glands, and uterus. We report that a targeted null mutation in the mK8 gene causes mid-gestational lethality. Mutant embryos are growth retarded and suffer from internal bleeding, with an abnormal accumulation of erythrocytes in fetal livers. The mK8- phenotype has 94% penetrance, with a few mice surviving into adulthood. We suggest that mK8/mK18 filaments are important for the integrity of the fetal liver, like specialized human epidermal keratins for the integrity of the epidermis. This phenotype in mice differs from the reported function of simple epithelium keratins in Xenopus at the gastrulation stage. In mice, mK8 fulfills a vital function at 12 days postcoitum.
We have labelled precursor cells in the embryonic rat cerebral cortex using BAG, a retroviral vector that expresses beta-galactosidase. We had previously reported that labelled precursor cells generate clusters of labelled cells that could be classified into four types by their morphological appearance and anatomical distribution (Price and Thurlow, 1988). In this study, we have used immunohistochemistry and intracellular dye labelling to identify the cell types that make up these clusters. We discovered that clusters are almost always composed of a single cell type. In addition to clusters composed entirely of neurones, we found four different types of glial cell clusters. In the grey matter, glial clusters are composed either of protoplasmic astrocytes, or of cells that have an astrocyte morphology, but no glial filaments. In the white matter, clusters are composed of either fibrous astrocytes or oligodendocytes. Our results indicate that each of these different cortical cell types is generated from a separate population of precursor cells.
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In this article I describe what I see as the sources of confusion in the description and interpretation of cell lineage data. I concentrate on lineage in the nervous system, since that is my interest, but most of the arguments are broadly applicable. Since there are these differences between workers in the field, all will not agree with my perspective, but perhaps a consensus can evolve from the discussion. I see the problem as having two facets: First, there is a confusion surrounding terminology, which leads to too many different types of studies to be considered as studies of cell lineage; and second, there is some confusion about what can validly be concluded from a study of cell lineage.
This study explored the information-seeking behavior of 257 cancer patients or their relatives who received specific, treatment-related information from the Illinois office of the Cancer Information Service (CIS); it also explored the information-seeking behavior of a sample of 262 other cancer patients matched for age, gender, race, cancer site, and type of hospital where first seen. Among the matched patients, 53% sought information from at least one source besides their physicians. These information seekers were similar to the selected CIS patients in many respects. Compared with patients who did not seek information, both CIS patients and these other information seekers were more likely to have felt more stressed when first diagnosed, to have sought a second opinion, to have been seen at more hospitals and by more physicians since diagnosis, to prefer greater information about and involvement in their treatment plans, and to have been less confident that physicians always have the most current cancer knowledge. The majority of both information-seeking groups sought explanatory information about their cancer or treatment, and most wanted information just after their diagnosis and before starting treatment. Those in the comparison sample, however, had less well-defined questions and consulted fewer sources; only a few of them received the type of information provided by the CIS, and they were less likely to discuss with their physicians the information obtained from various sources.
Outcome in terms of progression of Korsakoff's psychosis is known to be unlikely when the preceding thiamin deficiency syndrome, Wernicke's encephalopathy, does not follow heavy alcohol use. There is evidence that alcohol potentiates thiamin-related brain damage. It is argued here that in heavy drinkers, if vomiting precedes the onset of the encephalopathy, then the latter might develop at a time when tissue alcohol levels are close to zero. Any progression to Korsakoff's psychosis could then be associated with less or even no impairment. This outcome would not be expected if ingestion of alcohol continued during the vomiting stage. In a follow-up study of 61 cases of alcoholic Wernicke's encephalopathy, these concepts are given some support by the results obtained.