Academic literature on the topic 'Murnau (Concentration camp)'

Fluoride has made an enormous contribution to declines in dental caries (Kidd 2005; Murray and Naylor 1996). Fissure sealants are a proven preventive agent. This chapter provides a brief overview of the history of fluoride and presents a brief synopsis of the mode of action, method of delivery, safety, and controversies in the use of fluoride. A public health perspective on fissure sealants will also be presented. An account of the history of fluoride can be found in Kidd (2005) and Murray et al. (2003) and is summarized in this section (see Box 12.1 for key dates). In 1901, Frederick McKay, a dentist in Colorado Springs, USA, noticed that many of his patients, who had spent all their lives in the area, had a distinctive stain on their teeth known locally as ‘Colorado stain’. McKay was puzzled and called in the assistance of a dental researcher G.V. Black. They found that other communities in the USA had the characteristic mottling. Their histological examination of affected teeth showed that the enamel was imperfectly calcified, but that decay in the mottled teeth was no higher than in normal teeth. McKay suspected that something in the water supply was producing the brown stain, and more evidence came from Bauxite, a community formed to house workers of a subsidiary of the Aluminium Company of America (ALCOA). A local dentist noticed that children in Bauxite had mottled teeth, whereas children in nearby Benton did not. McKay investigated the problem but was unable to find a cause for the staining when the water supply was tested. In 1933, Mr H.V. Churchill, Chief Chemist for ALCOA (anxious that aluminium would not be blamed for the mottling), analysed the water and found that the fluoride ion concentration in the water supply of the Bauxite community was abnormally high (13.7 ppm). He tested other communities affected by mottling which had been previously identified by McKay and found that they too had high levels of fluoride present in the water supplies.

Vulnerable plaques are inflamed, active, and growing lesions which are prone to complications such as rupture, luminal and mural thrombosis, intraplaque hemorrhage, and rapid progression to stenosis. It remains difficult to assess what factors influence the biomechanical stability of vulnerable plaques and promote some of them to rupture while others remain intact. The rupture of thin fibrous cap overlying the necrotic core of a vulnerable plaque is the principal cause of acute coronary syndrome. The mechanism or mechanisms responsible for the sudden conversion of a stable atherosclerotic plaque to a life threatening athero-thrombotic lesion are not fully understood. It has been widely assumed that plaque morphology is the major determinant of clinical outcome [1, 2]. Thin-cap fibroatheroma with a large necrotic core and a fibrous cap of < 65μm was describes as a more specific precursor of plaque rupture due to tissue stress.