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Your search keyword '"Thompson, Philip J."' showing total 17 results
Start Over Author "Thompson, Philip J." Publisher american thoracic society
17 results on '"Thompson, Philip J."'

2. Influenza A/H1N1_09: Australia and New Zealand's Winter of Discontent

Author

Kotsimbos, Tom, Waterer, Grant, Jenkins, Christine, Kelly, Paul, Cheng, Allen, Hancox, Robert J, Holmes, Mark, Wood-Baker, Richard, Bowler, Simon, Irving, Louis, Thompson, Philip J, Kotsimbos, Tom, Waterer, Grant, Jenkins, Christine, Kelly, Paul, Cheng, Allen, Hancox, Robert J, Holmes, Mark, Wood-Baker, Richard, Bowler, Simon, Irving, Louis, and Thompson, Philip J

Abstract

Influenza A/H1N1-09 emerged in Mexico at the end of the Northern Hemisphere winter.Within weeks, the focus shifted to the Southern Hemisphere as the introduction of the novel virus coincided with the beginning of the influenza season. Intensive public health and health services planning had occurred in Australia and New Zealand as preparation for an influenza pandemic before 2009. However, this first pandemic wave was quite different to what had been expected. Key elements of the pandemic and response are outlined from the perspective of clinicians working at the frontline of patient care. In particular, they examine why past influenza pandemics and recent history are poor predictors of the current pandemic, the discordance between potential for transmission and disease severity, the broad clinical spectrum of H1N1-09 infection, clinical and health service management issues, and the relationship between health care and government policy. Finally, they address the need for the respiratory community to show leadership in times of crisis. Lessons learned in Australia and New Zealand during 2009 have important messages for similarly resourced countries in the Northern Hemisphere in the coming months as they face their own influenza season.

Published
2010

11. Categorizing Asthma Severity

Author

COLICE, GENE L., primary, BURGT, JENNIFER VANDEN, additional, SONG, JESSIE, additional, STAMPONE, PATTI, additional, and THOMPSON, PHILIP J., additional

Published
1999
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16. Angiotensin-Converting Enzyme

Author

Thompson, Philip J., primary, Kemp, Michael W., additional, McAllister, William A.C., additional, Al Habet, Saed M.H., additional, and Turner-Warwick, Margaret E.H., additional

Published
1986
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17. Transforming growth factor beta induces vascular endothelial growth factor elaboration from pleural mesothelial cells in vivo and in vitro.

Author

Gary Lee YC, Melkerneker D, Thompson PJ, Light RW, and Lane KB

Subjects
Analysis of Variance, Animals, Dose-Response Relationship, Drug, Doxycycline pharmacology, Doxycycline therapeutic use, Drug Evaluation, Preclinical, L-Lactate Dehydrogenase analysis, Leukocyte Count, Linear Models, Mice, Mice, Inbred C57BL, Pleural Effusion chemistry, Pleural Effusion cytology, Proteins analysis, Rabbits, Talc pharmacology, Talc therapeutic use, Transforming Growth Factor beta pharmacology, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factors, Capillary Permeability drug effects, Capillary Permeability physiology, Disease Models, Animal, Endothelial Growth Factors physiology, Epithelium drug effects, Epithelium metabolism, Lymphokines drug effects, Lymphokines physiology, Pleura cytology, Pleural Effusion drug therapy, Pleural Effusion etiology, Pleurodesis adverse effects, Pleurodesis methods, Transforming Growth Factor beta physiology, Transforming Growth Factor beta therapeutic use
Abstract

Vascular endothelial growth factor (VEGF) increases vascular permeability and is important in pleural effusion formation. In studies using transforming growth factor beta (TGF-beta) to produce pleurodesis, we observed that although TGF-beta was more effective than talc or doxycycline, it induced transient production of large pleural effusions. We hypothesized that TGF-beta stimulates VEGF production in pleural tissues in vivo, and by mesothelial cells in vitro. New Zealand White rabbits (n = 33) were given TGF-beta(2) (1.7 or 5.0 microg), talc (400 mg/kg), doxycycline (10 mg/kg), or buffer intrapleurally. Pleural fluid was collected at 24 h. Intrapleural injection of TGF-beta(2) induced a dose-dependent increase in VEGF production. The pleural fluid VEGF level was 2-fold higher in rabbits given 5.0 microg of TGF-beta(2) than in those given 1.7 microg of TGF-beta(2) and 3-fold higher than in those given buffer. VEGF levels were higher after the injection of TGF-beta(2) than after administration of talc or doxycycline. The pleural fluid VEGF correlated significantly with the volume of pleural effusions (r = 0.79, p < 0.00001). In vitro, TGF-beta(2) stimulated a dose-dependent increase in VEGF production from murine pleural mesothelial cells. At 4 and 24 h, TGF-beta(2), but not talc or doxycycline, induced a significant increase in VEGF, when compared with controls. The mesothelial cell VEGF production was significantly reduced by anti-TGF-beta antibody in the TGF-beta(2), talc, and control (buffer and medium) groups. In conclusion, mesothelial cells are an important source of VEGF. TGF-beta increases the VEGF production by mesothelial cells in vivo and in vitro.

Published
2002
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