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1

The effect of Aspirin on Gomori-positive glia in mouse brain

100%
Sura P., Srebro Z., Wilinski B., Goralska M.
Folia Biologica
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2008
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vol. 56
|
issue 1-2
73-75
EN
Aspirin (acetylsalicylic acid, ASA) treatment resulted in a significant decrease in the amount of the sulfur-rich Gomori-positive material present in the cytoplasm of periventricular glia. It also caused the accumulation of the Gomori-positive neurosecretory material in the supraoptic and paraventricular nuclei and, most pronounced, in the neurosecretory axons of the paraventricular- and supraoptic-neurophypophysial tract.
2

Expression profile analysis of human peripheral blood mononuclear cells in response to aspirin

88%
Choi S., Park H.-S., Cheon M. S., Lee K.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
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issue 2
151-158
EN
Aspirin is a popular nonsteroidal anti-inflammatory drug, but some patients suffer from hypersensitivity to it. This prompted us to identify the factors or molecules related to these responses. A commercially available DNA microarray was used to study changes in gene expression in human peripheral blood mononuclear cells (PBMCs) after aspirin treatment. The PBMCs were collected from a patient with aspirin-intolerant asthma and one normal healthy control. We identified 61 and 107 genes respectively induced and repressed by aspirin treatment in the PBMCs derived from the normal control. In the patient showing aspirin-induced asthma responses, 31 genes were up-regulated and 6 were down-regulated after aspirin treatment. Among these, 1 gene was expressed with the same pattern in the control and the patient. In contrast, 19 genes showed different expression patterns, and it turned out that most of them were involved in immune responses, cell growth/proliferation, transcription/ translation, and signaling pathways. These results show the molecules involved in hypersensitivity to aspirin and may lead to a better understanding of adverse responses to aspirin. Furthermore, they can provide clues for identifying novel therapeutic and/or preventive molecular targets of the adverse effects of aspirin.
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