A Challenge to the Reigning Theory of the Just War

Troubled times often gives rise to great art that reflects those troubles. So too with political theory. The greatest work of twentieth century political theory, John Rawls's A theory of justice, was inspired in various respects by extreme social and economic inequality, racialized slavery and racial segregation in the United States. Arguably the most influential work of political theory since Rawls—Michael Walzer's Just and unjust wars—a sustained and historically informed reflection on the morality of interstate armed conflict—was written in the midst of the Vietnam War. It should be no surprise, then, that the bellicose period of the past 20 years should give rise to a robust new literature in political theory on the morality of armed conflict. It has been of uneven quality, and to some extent episodic, responding to particular challenges—the increased prevalence of asymmetric warfare and the permissibility of preventive or preemptive war—that have arisen as a result of specific events. In the past decade, however, a group of philosophers has begun to pose more fundamental questions about the reigning theory of the morality of armed conflict warfare—just war theory—as formulated by Walzer and others. Jeff McMahan's concise, inventive and tightly argued work Killing in war is without doubt the most important of these challenges to the reigning theory of the just war. This review article discusses McMahan's work, some of the critical attention it has received, and its potential implications for practice

Graphical representation (distance plots) of the redundancy analysis (RDA) model of Hellinger-transformed OTU abundances.

<p>The model illustrate the relationship of gut microbes of healthy controls, individuals treated with ß-lactam antibiotic (Cephalosporins/Ampicillin/Sulbactam) and individuals treated with fluoroquinolones at DNA level.</p

Effects of β-Lactam Antibiotics and Fluoroquinolones on Human Gut Microbiota in Relation to <i>Clostridium difficile</i> Associated Diarrhea

<div><p><i>Clostridium difficile</i> infections are an emerging health problem in the modern hospital environment. Severe alterations of the gut microbiome with loss of resistance to colonization against <i>C. difficile</i> are thought to be the major trigger, but there is no clear concept of how <i>C. difficile</i> infection evolves and which microbiological factors are involved. We sequenced 16S rRNA amplicons generated from DNA and RNA/cDNA of fecal samples from three groups of individuals by FLX technology: (i) healthy controls (no antibiotic therapy); (ii) individuals receiving antibiotic therapy (Ampicillin/Sulbactam, cephalosporins, and fluoroquinolones with subsequent development of <i>C. difficile</i> infection or (iii) individuals receiving antibiotic therapy without <i>C. difficile</i> infection. We compared the effects of the three different antibiotic classes on the intestinal microbiome and the effects of alterations of the gut microbiome on <i>C. difficile</i> infection at the DNA (total microbiota) and rRNA (potentially active) levels. A comparison of antibiotic classes showed significant differences at DNA level, but not at RNA level. Among individuals that developed or did not develop a <i>C. difficile</i> infection under antibiotics we found no significant differences. We identified single species that were up- or down regulated in individuals receiving antibiotics who developed the infection compared to non-infected individuals. We found no significant differences in the global composition of the transcriptionally active gut microbiome associated with <i>C. difficile</i> infections. We suggest that up- and down regulation of specific bacterial species may be involved in colonization resistance against <i>C. difficile</i> providing a potential therapeutic approach through specific manipulation of the intestinal microbiome.</p></div