Scapegoat: John Dewey and the character education crisis

Many conservatives, including some conservative scholars, blame the ideas and influence of John Dewey for what has frequently been called a crisis of character, a catastrophic decline in moral behavior in the schools and society of North America. Dewey’s critics claim that he is responsible for the undermining of the kinds of instruction that could lead to the development of character and the strengthening of the will, and that his educational philosophy and example exert a ubiquitous and disastrous influence on students’ conceptions of moral behavior. This article sets forth the views of some of these critics and juxtaposes them with what Dewey actually believed and wrote regarding character education. The juxtaposition demonstrates that Dewey neither called for nor exemplified the kinds of character-eroding pedagogy his critics accuse him of championing; in addition, this paper highlights the ways in which Dewey argued consistently and convincingly that the pedagogical approaches advocated by his critics are the real culprits in the decline of character and moral education

Recruitment Constraints in Singapore's Fluted Giant Clam (Tridacna squamosa) Populations - A Dispersal Model Approach

10.1371/journal.pone.0058819PLoS ONE83

Resolution of inflammation: a new therapeutic frontier

Dysregulated inflammation is a central pathological process in diverse disease states. Traditionally, therapeutic approaches have sought to modulate the pro- or anti-inflammatory limbs of inflammation, with mixed success. However, insight into the pathways by which inflammation is resolved has highlighted novel opportunities to pharmacologically manipulate these processes — a strategy that might represent a complementary (and perhaps even superior) therapeutic approach. This Review discusses the state of the art in the biology of resolution of inflammation, highlighting the opportunities and challenges for translational research in this field

Ocrelizumab versus Interferon Beta-1a in Relapsing Multiple Sclerosis

Supported by F. Hoffmann–La Roche