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Dr Robert Knox was publicly scorned and disgraced for his unwitting involvement in the Burke and Hare serial murders in 1828. Far less appreciated is his brilliance as an anatomist and he espoused the European movement in Transcendental Anatomy, which aimed to uncover the laws governing what we now know as evolution and the origin of species. Knox fully embraced Transcendental Anatomy during a sojourn in Paris and taught it on his return to Edinburgh, where there was a critical mass of like-minded Transcendental Anatomists. Charles Darwin spent 1825–1827 as a medical student in Edinburgh when Transcendental Anatomy was at its peak amongst the city's anatomists, and evolution – then known as transmutation – was a source of great interest and controversy. Knox intended to research Transcendental Anatomy, but this was thwarted by conflicting demands on his time in the second half of the 1820s decade and the Burke and Hare tragedy. He did, however, go on to champion Transcendental Anatomy and write extensively on it. [ABSTRACT FROM AUTHOR]

Abstract Objective Diesel exhaust particulate (DEP), a major component of urban air pollution, has been linked to atherogenesis and precipitation of myocardial infarction. We hypothesized that DEP exposure would increase and destabilise atherosclerotic lesions in apolipoprotein E deficient (ApoE−/−) mice. Methods ApoE−/− mice were fed a ‘Western diet’ (8 weeks) to induce ‘complex’ atherosclerotic plaques, with parallel experiments in normal chow fed wild-type mice. During the last 4 weeks of feeding, mice received twice weekly instillation (oropharyngeal aspiration) of 35 μL DEP (1 mg/mL, SRM-2975) or vehicle (saline). Atherosclerotic burden was assessed by en-face staining of the thoracic aorta and histological examination of the brachiocephalic artery. Results Brachiocephalic atherosclerotic plaques were larger in ApoE−/− mice treated with DEP (59±10%) than in controls (32±7%; P = 0.017). In addition, DEP-treated mice had more plaques per section of artery (2.4±0.2 vs 1.8±0.2; P = 0.048) and buried fibrous layers (1.2±0.2 vs 0.4±0.1; P = 0.028). These changes were associated with lung inflammation and increased antioxidant gene expression in the liver, but not with changes in endothelial function, plasma lipids or systemic inflammation. Conclusions Increased atherosclerosis is caused by the particulate component of diesel exhaust producing advanced plaques with a potentially more vulnerable phenotype. These results are consistent with the suggestion that removal of the particulate component would reduce the adverse cardiovascular effects of diesel exhaust.

Richard Muir (1862—1931) began his career as a 'lab boy' in the Pathology Department of the University of Edinburgh in 1876 at the age of 13. This was a newly created category of worker that eventually became today's biomedical scientist Muir rapidly gained expertise in pathological and bacteriological techniques including staining and microscopy. Exceptionally, for someone non-medical and non-university-educated individual, he was elected a member of the Pathological Society of Great Britain and appointed Demonstrator in Pathology in the University of Edinburgh Pathology Department. He authored papers on staining techniques for bacteria and on the pathology of syphilis of the ear and became a recognised diagnostic histopathologist, despite having no medical qualifications. He especially excelled as an artist, depicting the microscopic world of pathology and microbiology and produced diagrams for hundreds of publications including his own book and also large wall hangings of the microscopic world for teaching purposes. This paper describes the unique contribution of Richard Muir to pathology in Edinburgh and beyond in the early 20th century. [ABSTRACT FROM AUTHOR]

The various ischemic and thrombotic effects of dilute diesel-exhaust and air pollution on the different functions in men with coronary heart disease are studied. The analysis reveals that the exposure to combustion-derived air pollution leads to several cardiovascular problems in men.

Abstract In their work on human cancer, the International Agency for Research on Cancer have run a programme of <> that evaluate carcinogenic risk of chemicals to man. The data [...]

Regulation of LPS-mediated inflammation in vivo and in vitro by the thiol antioxidant Nacystelyn. Am J Physiol Lung Cell Mol Physiol 286: L1319-L1327, 2004; 10.1152/ajplung.00329. 2003.--Increased levels of proinflammatory cytokines are present in bronchoalveolar lavage fluid in various lung diseases. Redox-sensitive transcription factors such as NF-[kappa]B regulate gene transcription for these cytokines. We therefore studied the effect of a new thiol antioxidant compound, Nacystelyn (NAL), on IL-8 regulation in a human macrophage-derived cell line (THP-1). LPS (10 [micro]g/ml) increased IL-8 release compared with control levels. This LPS activation was inhibited by coincubation with NAL (1 and 5 mM). Pretreatment with cycloheximide or okadaic acid, protein synthesis, and serine/threonine phosphatase inhibitors, respectively, did not modify inhibition of IL-8 release caused by NAL. NF-[kappa]B and C/EBP DNA binding were increased after LPS treatment compared with control, an effect inhibited by cotreatment with NAL. Activator protein (AP)-1 DNA binding was unaffected. The enhanced neutrophil chemotaxis produced by conditioned media from LPS-treated cells was inhibited when cells were cotreated with NAL. The selectivity of NAL inhibition upon IL-8 expression was studied. LPS-treated THP-1 cells also had higher levels of TNF-[alpha], transforming growth factor (TGF)-[beta]1 and -3, MIP-1[alpha] and -[beta], and RANTES gene expression. However, only LPS-induced IL-8 and TGF-[beta]1 expressions were inhibited by NAL. An anti-inflammatory effect of NAL was confirmed in vivo as shown by a reduction in LPS-induced neutrophil recruitment to the lungs following instillation of NAL into the lungs. Our studies demonstrate that NAL has anti-inflammatory properties in vitro and in vivo, may therefore have a therapeutic role in lung inflammation, and has the advantage over other antioxidant agents in that it may be administrated by inhalation. interleukin-8; lipopolysaccharide; THP-l cells