1,721,725 research outputs found
O'Brien, T, VX36898
This record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/408311Surname: O'BRIEN. Given Name(s) or Initials: T. Military Service Number or Last Known Location: VX36898. Missing, Wounded and Prisoner of War Enquiry Card Index Number: 40852.237474
Item: [2016.0049.40586] "O'Brien, T, VX36898
O'Brien, T L, VX45873
This record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/408315Surname: O'BRIEN. Given Name(s) or Initials: T L. Military Service Number or Last Known Location: VX45873. Missing, Wounded and Prisoner of War Enquiry Card Index Number: 13525.237478
Item: [2016.0049.40590] "O'Brien, T L, VX45873
O'Brien, T R (Thomas Raymond), VX18312
This record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/408306Surname: O'BRIEN. Given Name(s) or Initials: T R (THOMAS RAYMOND). Military Service Number or Last Known Location: VX18312. Missing, Wounded and Prisoner of War Enquiry Card Index Number: 32840.237469
Item: [2016.0049.40581] "O'Brien, T R (Thomas Raymond), VX18312
O'Brien, T R (Terence Robert William Patrick), NX60147
This record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/408284Surname: O'BRIEN. Given Name(s) or Initials: T R (TERENCE ROBERT WILLIAM PATRICK). Military Service Number or Last Known Location: NX60147. Missing, Wounded and Prisoner of War Enquiry Card Index Number: 14498.237447
Item: [2016.0049.40559] "O'Brien, T R (Terence Robert William Patrick), NX60147
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Adenoviral-mediated overexpression of catalase inhibits endothelial cell proliferation
Although hydrogen peroxide (H(2)O(2)) induces proliferation of vascular smooth muscle cells, its role in endothelial cell proliferation is unclear. Our aim was to study the role of hydrogen peroxide in endothelial cell proliferation by overexpressing catalase. Human aortic endothelial cells were transduced with adenoviral vectors encoding beta-galactosidase (Adbetagal) or catalase (AdCat) or were exposed to diluent alone (control). Transgene expression was demonstrated by beta-galactosidase staining, Western analysis, and significantly increased enzyme activity in AdCat-transduced cells. Overexpression of catalase decreased DNA synthesis in AdCat compared with control and Adbetagal-transduced cells (536.8 +/- 31 vs. 1,875.1 +/- 132.9 vs. 1,347.5 +/- 93.7 dpm/well, respectively; P < 0.05 vs. control and Adbetagal). Six days after transduction with AdCat (multiplicity of infection = 50), cell numbers were significantly reduced (AdCat: 38 +/- 1.8% of cell counts in control, P < 0.05; and 45 +/- 2% of cell count in Adbetagal, P < 0.05). Incubation with aminotriazole 10 mmol/l, an inhibitor of catalase, prevented this effect. The number of apoptotic cells was increased one- and threefold 2 and 4 days, respectively, after transduction with AdCat. Exogenous administration of low concentrations of H(2)O(2) (50 microM) significantly increased cell proliferation, whereas it was inhibited by higher concentrations. These results suggest that H(2)O(2) is an important modulator of endothelial cell proliferation
Expression and function of recombinant endothelial nitric oxide synthase in human endothelial cells
Endothelial dysfunction is frequently involved in the pathogenesis of vascular disease. While nitric oxide (NO) inhibits smooth muscle cell proliferation, its effect on endothelial cell proliferation is unclear. The aim of this study was to determine if adenoviral-mediated gene transfer of endothelial NO synthase (eNOS) to human umbilical vein endothelial cells (HUVECs) would result in increased generation of NO and affect endothelial cell proliferation. HUVECs were transduced with adenoviral vectors encoding eNOS (AdeNOS) or beta-galactosidase (Ad beta gal) or exposed to diluent (control). AdeNOS-transduced cells showed increased eNOS expression as detected by Western blot analysis, and increased concentrations of cGMP (control 0.7 +/- 0.1; Ad beta gal 0.9 +/- 0.2; AdeNOS 3.1 +/- 0.5 pmol/mg protein; p < 0.001) and nitrite (control 11.8 +/- 1.2; Ad beta gal 13.3 +/- 1.7; AdeNOS 21.1 +/- 2.2 nmol/mg protein/hour; p < 0.01). DNA synthesis as assessed by [(3)H]thymidine incorporation and cell counts were significantly reduced (by approximately 30%) in AdeNOS-transduced HUVECs. Expression of mitogen-activated protein kinase was also decreased in AdeNOS-transduced cells. This study shows that adenoviral-mediated gene transfer of eNOS to HUVECs inhibits endothelial cell proliferation
- …
