1994 Fiscal Year Final Research Report Summary
Pathogenesis of Pulmonary Emphysema
| Project/Area Number |
05670539
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Toky Women's Medical College |
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Principal Investigator |
NAGAI Atsushi Tokyo Women's Medical College, Associate Professor, 医学部, 助教授 (60101820)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUMIYA Haruko Tokyo Women's Medical College, Instructor, 医学部, 助手 (70266716)
KAMEYAMA Shinkichi Tokyo Women's Medical College, Instructor, 医学部, 助手 (50214557)
AOSHIBA Kazutetsu Tokyo Women's Medical College, Instructor, 医学部, 助手 (60231776)
INANO Hidetaka Tokyo Women's Medical College, Instructor, 医学部, 助手 (40191887)
YASUI Shuji Tokyo Women's Medical College, Assistant Professor, 医学部, 講師 (30147392)
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| Project Period (FY) |
1993 – 1994
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| Keywords | Emphysema / Lung injury / Oxidant / Elastase / Niacin / Nicotinamide / DNA damage / Apoptosis |
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| Research Abstract |
Neutrophil
1. Effects of nicotine in the tabacco smoke on neutrophil survival were investigated. Neutrophil survival prolonged with nicotine in dose related fashion. A transmission electron microscopy and electrophoresis of the exracted DNA revealed that nicotine inhibits neutrophil apoptosis.
2. Filtrability of neutrophils exposed to tabacco smoke was investigated. Neutrophils exposed to the smoke showed ultrastructural abnormalities and a decreased filtrability. The decrease in filtrability was due to exposure of oxidants in the gas components of the smoke. Nicotine prevented the decrease in concentration dependent fashion and the effect of nicotine was due to antioxidant effects.
Lung injury induced by oxidant
1. Lung injury induced by oxidant was inhibited by niacin or nicotinamide. These agents prevented a decrease in NAD which was induced by oxidant exposure.
2. Cultured bronchial epithelial cells were damaged by H202 exposure in concentration- and time-dependent fashion. The epithelial damage induced by H202 was inhibited by an addition of niacin, nicotinamide, theophilline, or DBcAMP.Niacin inhibited a decrease in intracellular ATP which was brought about by H202 exposure.
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Research Products
(12 results)
