Plants of Western New South Wales grew from the long experience and expertise which the authors acquired during their employment with their respective organisations in the arid and semi-arid pastoral areas of the State. Each author became aware of the need for a comprehensive record illustrating and describing the great array of plants in the area. The need was identified both for people involved in research and advisory services, and particularly for the landholders who need to manage the plants for their livelihood. The book is a landmark because it draws together all of the existing knowledge of plants from the area, adds to it the extensive collections and research of the authors and presents the whole as a comprehensive collation and description of the plants of the dry pastoral portion of the State. Because of its comprehensive nature, the work is significant to pastoralists and people concerned with plants throughout Australia. The 1992 edition of Plants of Western New South Wales has been reprinted and published by CSIRO PUBLISHING with a one page appendix giving website addresses of various herbaria in Australia where the reader can readily access up-to-date information on botanical name changes.
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) are commonly used to control pain, inflammation, and limit the cardinal signs of injury in humans. However, prolonged use of NSAIDs increases the risk of heart attack (myocardial infarction; MI) and the subsequent risk of heart and renal failure. The molecular and cellular mechanism of action for this adverse effect, particularly along the cardiorenal network, is incomplete. To define the mechanism, carprofen (CAP), an NSAID was administered at the dose of 5 mg/kg to C57BL/6 male mice for two weeks. After last dose of CAP treatment mice were subjected to permanent occlusion of coronary artery that induces irreversible cardiac remodeling while maintaining naive and MI-controls. After MI, cardiac pathology and dysfunction were confirmed, along with additional measurements of kidney function, histology, and injury markers, such as plasma creatinine. CAP treatment increased plasma creatinine levels and subsequently, myocardial structural disorganization increased. Kidney neutrophil gelatinase associated lipocalin (NGAL) and protein expression were increased post-MI. After two weeks CAP treatment, the expression of pyrogenic pro-inflammatory cytokines TNF-α and IL-1β were increased compared to non-CAP treated mice, indicative of amplified inflammatory response. There was also evidence that renal injury of both the post-CAP treatment controls and post-CAP MI were much greater than the non-CAP treated naïve controls, as serum creatinine and NGAL levels were elevated along with obvious structural impairment of the glomerulus. Therefore, CAP treatment tampers with the acute inflammatory response that promotes cardiorenal syndrome and non-resolving inflammation post-MI in acute heart failure.
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