The intratracheal administration of endotoxin: X. Dexamethasone downregulates neutrophil emigration and cytokine expression in vivo

Intratracheal instillation of endotoxin (LPS) causes acute pulmonary inflammation characterized by the accumulation of plasma proteins and leukocytes within the pulmonary airways. The synthetic glucocorticoid dexamethasone 1) inhibits the LPS-initiated vascular leak of plasma proteins into the airspace, 2) inhibits the LPS-initiated emigration of neutrophils and lymphocytes into the airspace in a dose-dependent fashion, and 3) inhibits LPS-initiated mRNA and/or bronchoalveolar lavage protein expression of cytokines (TNF, IL-1 and IL-6) and chemokines (MIP-l α , MIP-2 and MCP-1). In conclusion, dexamethasone inhibits both the vascular and cellular aspects of acute inflammation by downregulation of a broad spectrum of inflammatory cytokines and chemokines.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44515/1/10753_2005_Article_BF01487403.pd

The “Fishing License” method for analyzing the time course of effects in repeated measurements.

[[sponsorship]]統計科學研究所[[note]]已出版;[SCI];有審查制度;具代表性[[note]]http://gateway.isiknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=Drexel&SrcApp=hagerty_opac&KeyRecord=0277-6715&DestApp=JCR&RQ=IF_CAT_BOXPLO

The Search for Non-Linear Exposure-Response Relationships at Ambient Levels in Environmental Epidemiology

Environmental exposures to ambient air particulate matter (PM), ozone (O3), environmental tobacco smoke (ETS), and to dioxin and related compounds are of considerable public health concern, and risk assessments for them have generally been based on linear, non-threshold models derived from epidemiological study data. While the epidemiological databases for PM, O3, and ETS have been sufficient to show that adverse health effects are occurring, the relative risks have been quite low, and it has not been possible, to date, to identify thresholds or non-linear relationships for them. For dioxin and related compounds, the evidence for excess cancer risks has been inadequate to establish causality, and there is suggestive evidence that hormesis may have occurred