Biomedical subjects
K A Bailey
Publications and source records attributed to K A Bailey.
Regulation of neural precursor differentiation in the embryonic and adult forebrain.
1. Precursors form the neuroepithelium of the developing cortex and also from the adult sub-ventricular zone, can be cloned in vitro after stimulation with fibroblast growth factor (FGF)-2 and have the potential to give rise to both neurons and glia. The generation of neurons from these clones can be stimulated by either a factor derived from an astrocyteprecursor line, Ast-1, or FGF-1. 2. Neuronal differentiation stimulated by FGF-1 can be inhibited by diacylglycerol-lipase inhibitor and mimicked by arachidonic acid, suggesting that the neuronal differentiation is signalled through the PCL gamma pathway. 3. The sequential expression of FGF-2 and FGF-1 within the developing forebrain neuroepithelium fits with the different functions the two FGF play in precursor regulation. 4. We have shown that the precursor response to FGF-1 is regulated by a heparan sulphate proteoglycan (HSPG) expressed within the developing neuroepithelium. Precursors restricted to the astrocyte cell lineage can be stimulated by epidermal growth factor or FGF-2; however, the differentiation into GFAP positive astrocytes appears to require a cytokine acting through the leukaemia inhibitory factor beta receptor.
Virulence of a Porphyromonas gingivalis W83 mutant defective in the prtH gene.
In a previous study we cloned and determined the nucleotide sequence of the prtH gene from Porphyromonas gingivalis W83. This gene specifies a 97-kDa protease which is normally found in the membrane vesicles produced by P. gingivalis and which cleaves the C3 complement protein under defined conditions. We developed a novel ermF-ermAM antibiotic resistance gene cassette, which was used with the cloned prtH gene to prepare an insertionally inactivated allele of this gene. This genetic construct was introduced by electroporation into P. gingivalis W83 in order to create a protease-deficient mutant by recombinational allelic exchange. The mutant strain, designated V2296, was compared with the parent strain W83 for proteolytic activity and virulence. Extracellular protein preparations from V2296 showed decreased proteolytic activity compared with preparations from W83. Casein substrate zymography revealed that the 97-kDa proteolytic component as well as a 45-kDa protease was missing in the mutant. In in vivo experiments using a mouse model, V2296 was dramatically reduced in virulence compared with the wild-type W83 strain. A molecular survey of several clinical isolates of P. gingivalis using the prtH gene as a probe suggested that prtH gene sequences were conserved and that they may have been present in multiple copies. Two of 10 isolates did not hybridize with the prtH gene probe. These strains, like the V2296 mutant, also displayed decreased virulence in the mouse model. Taken together, these results suggest an important role for P. gingivalis proteases in soft tissue infections and specifically indicate that the prtH gene product is a virulence factor.
Neuronal progenitors identified by their inability to express class I histocompatibility antigens in response to interferon-gamma.
Interferon-gamma (IFN-gamma) can induce class I major histocompatibility complex (MHC) antigen (H-2) expression on virtually all neuroepithelial cells isolated from embryonic day 9 (E9) mice. However, a subpopulation of cells become refractory to H-2 induction (H-21-) by E10 and the percentage of H-2 noninducible cells increases during development. Cell sorting, by flow cytometry or magnetic bead immunoselection, has shown that H-21- cells give rise exclusively to neuronal cells, and by E12, the majority of the neuronal progenitors are found within this population. It has also been found that 98% of the H-21- also express the neuron-associated marker, A2B5. Cells of the glial cell lineage retain the ability to express class I antigens throughout development. From these studies, it is clear that the neuroepithelium contains cells committed to the neuronal cell lineage as early as E10 in the mouse.
The pattern of diagnosed HIV infection in Australia, 1984-1992.
OBJECTIVE: To describe the pattern of newly diagnosed HIV infection in Australia, between 1984 and 1992. METHODS: State and Territory health authorities reported cases of newly diagnosed HIV infection to the national HIV surveillance centre. Information sought on each case included the State or Territory of diagnosis, the case identifying number, the sex, date of birth and postcode of residence of the person with newly diagnosed HIV infection, the source of exposure to HIV and the date of specimen collection for the diagnosis of infection. RESULTS: By the end of December 1992, a total of 16,765 cases of newly diagnosed HIV infection had been reported in Australia. The annual number of cases declined between 1985 and 1992. Most diagnoses were among males, and exposure to HIV was attributed to male homosexual contact for more than 80% of cases for which information on exposure to HIV was available. Cases of HIV infection attributed to heterosexual contact represented an increasing proportion of the annual number of diagnoses over the period 1985-1992, among both men and women. CONCLUSION: National surveillance for newly diagnosed HIV infection has complemented national surveillance for diagnoses of AIDS as a key mechanism for monitoring the course of the HIV epidemic in Australia. The pattern of newly diagnosed HIV infection was similar to the pattern of AIDS diagnoses, with the overwhelming majority of diagnoses of infection being in adult males whose exposure to HIV was attributed to homosexual contact. Limitations of HIV surveillance include the lack of information on HIV testing patterns, incomplete information on HIV exposure histories and duplication of reported diagnoses.
Allergy testing.
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The acquired immunodeficiency syndrome in Australia: incidence 1982-1991.
OBJECTIVE: To describe the incidence of the acquired immunodeficiency syndrome (AIDS) in Australia between 1982 and 1991. DESIGN: State and Territory Health Departments notified new diagnoses of AIDS to the National AIDS Registry. Information reported for each case included sex, date of birth, date of AIDS diagnosis, presumed mode of exposure to the human immunodeficiency virus (HIV), and illness(es) on which the diagnosis of AIDS was based. RESULTS: To the end of March 1992, 3,160 cases of AIDS were reported as having been diagnosed between 1982 and the end of 1991. The cumulative incidence per head of population was about twice as high in New South Wales as in Australia as a whole. Over 97% of cases were in men, of whom 91% were adults or adolescents reporting homosexual contact. In women, 40% of cases were acquired through receipt of blood, blood products or tissue. The annual incidence of AIDS rose sharply until about 1988, but the annual rates of increase slowed in subsequent years. This trend was also apparent in cases acquired through sexual contact between men. In other exposure groups, numbers of cases were much smaller and trends less apparent. However, there was no indication of a similar levelling in AIDS incidence, except among blood transfusion recipients, in whom incidence may be declining. CONCLUSION: Transmission of HIV among people with AIDS in Australia has been overwhelmingly attributed to sexual contact between men. The annual incidence of cases attributed to sexual contact between men appears to be stabilising.
A method for the isolation of purified murine neuroepithelial cells from the developing mouse brain.
The adult mammalian central nervous system develops from the pseudostratified neuroepithelium of the neural tube. In order to study, in vitro, the differentiation of the neuroepithelial cells in detail and to identify factors that may influence this process, an uncontaminated, viable population of neuroepithelial cells, that still retains full developmental potential, is required. In this paper we describe a highly efficient method, involving differential trypsinization and micro-dissection, to cleanly separate the neuroepithelium from surrounding mesenchyme and ectoderm. The purity of isolated neuroepithelium has been assessed by monitoring for the presence of endothelial cells using an anti-endothelial antibody, MTS-12, and found to contain no significant level of contamination. Neuroepithelial cells prepared by this method have been demonstrated to divide and differentiate in tissue culture, to act as target cells for immortalization by proto-oncogenes and to differentiate into neurons in neural transplantation studies.
Allograft rejection overcome by immunoselection of neuronal precursor cells.
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What stimulates atrial natriuretic factor release during exercise?
Prior studies have shown that circulating atrial natriuretic factor (ANF) increases during short-term exercise, but the mechanism controlling ANF release, as well as the effect of exercise training on ANF release, remains unclear. Fifteen healthy mongrel dogs underwent short-term exercise testing before and after a 12-week period of exercise training (n = 8) or cage confinement (n = 7). ANF, norepinephrine, epinephrine, right atrial pressure, and heart rate were measured simultaneously at rest and during exercise at the time of each acute exercise study. Data were analyzed for all animals with normal baseline ANF values. Exercise training had no modulating effect on circulating ANF levels at rest or during exercise. Therefore, data before and after exercise training or cage confinement were grouped (n = 24) to determine the effects of short-term exercise. ANF levels increased from 49 +/- 2 pg/ml at rest to 60 +/- 4 pg/ml during exercise (p less than 0.05). Heart rate, norepinephrine, and epinephrine values also increased, but right atrial pressure actually decreased from 2.3 +/- 0.9 mm Hg at rest to -3.8 +/- 0.9 mm Hg during exercise (p less than 0.05). There was no correlation between ANF concentrations and levels of these other variables either at rest of during exercise. By demonstrating an increase in ANF with a simultaneous decrease in right atrial pressure, this study clearly shows that increased right atrial pressure is not the secretory stimulus for ANF release during exercise in the normal dog. The lack of correlation between ANF and right atrial pressure, heart rate, norepinephrine, and epinephrine levels suggests that factors other than these variables stimulate ANF release during short-term exercise.
Expression of MHC antigens in the central nervous system.
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Immortalization of mouse neural precursor cells by the c-myc oncogene.
Immortalized cell lines have been generated from embryonic mouse neuroepithelium by infection with a retrovirus containing the c-myc oncogene. The morphology and the antigenic phenotype of the cloned cell lines are characteristic of normal neuroepithelium. Although the cell lines are stable and do not spontaneously differentiate, morphological changes can be induced with both acidic and basic fibroblast growth factor. Fibroblast growth factor at 5 ng/ml stimulates differentiation of the neuroepithelial cells, and it has been shown that the cloned cell line 2.3D can differentiate into astrocytes, containing glial fibrillary acidic protein, and neurons, expressing the A2B5 marker and neurofilaments. This indicates that some cells in the neuroepithelium at embryonic day 10 are multipotent and are not restricted to either the glial or neuronal cell lineage. The cell lines also can be induced with interferon gamma to express class I and class II histocompatibility antigens. The response of the c-myc-immortalized cell lines to these two factors is similar to that observed with freshly isolated neuroepithelium and suggests that such immortalized precursor populations are representative of the cells found in the developing neuroepithelium.
Acrylonitrile and tissue glutathione: differential effect of acute and chronic interactions.
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