This book explores existing and potential strategies for using the genome sequences of human, mouse, other vertebrates and human pathogens to solve key problems in the treatment of immunological diseases and chronic infections. The assembled genome sequences now provide important opportunities for solving these problems, but a major bottleneck is the identification of key sequences and circuits controlling the relevant immune reactions. This will require innovative, interdisciplinary and collaborative strategies of a scale and complexity we are only now beginning to comprehend. Specific problems addressed include the following: What kinds of information are we lacking to understand how the genome sequence specifies the differentiation and response of immune system cells, and system behaviour such as immunological memory and tolerance? Which genome sequences and cellular circuits cause or prevent pathological immune responses to foreign pathogens, allergens or self-tissues? Which host and pathogen genome sequences and cellular circuits explain the failure of sterilizing immune responses to sophisticated human pathogens such as the agents of tuberculosis, malaria, metazoan parasites and chronic viruses? Containing contributions from a range of leading experts in the field, this book provides an important new perspective for clinical immunologists and basic researchers alike.

Ronald Fisher needed to develop elaborate models of genetic effects in order to set the foundations of Quantitative Genetics in his 1918 paper “The correlation between relatives on the supposition of Mendelian inheritance”. Since then, many significant implementations have been made to model genetic effects. However, at the verge of one century after Fisher’s kick-off, models of genetic effects keep on being discussed and implemented. Indeed, the relatively recent advent of QTL analyses challenged the state of the art of this field by providing researchers the opportunity to obtain and analyze estimates of genetic effects from real data. In this context, the development of this field was not exempt of some polemics, like the debate about the convenience of the functional and the statistical epistasis approaches. This research topic is meant to provide recent developments in models and estimation of genetic effects and to enrich the discussion about how and why models of genetic effects must be further developed and applied. The articles in this Research Topic shall thus extend, refine and/or provide a refresh look at Fisher’s original models of genetic effects and their application to genetic effects estimation and to improve our understanding of evolutionary processes and breeding programs.

The Janeway's Immunobiology CD-ROM, Immunobiology Interactive, is included with each book, and can be purchased separately. It contains animations and videos with voiceover narration, as well as the figures from the text for presentation purposes.

This casebook collects 64 case studies each of which raises an important and difficult ethical issue connected with planning, reviewing or conducting health-related research. The book's purpose is to contribute to thoughtful analysis of these issues by researchers and members of research ethics committees (REC's known in some places as ethical review committees or institutional review boards) particularly those involved with studies that are conducted or sponsored internationally. . This collection is envisioned principally as a tool to aid educational programs from short workshops on research.

The literature on recoding is scattered, so this superb book ?lls a need by prov- ing up-to-date, comprehensive, authoritative reviews of the many kinds of recoding phenomena. Between 1961 and 1966 my colleagues and I deciphered the genetic code in Escherichia coli and showed that the genetic code is the same in E. coli, Xenopus laevis, and guinea pig tissues. These results showed that the code has been c- served during evolution and strongly suggested that the code appeared very early during biological evolution, that all forms of life on earth descended from a c- mon ancestor, and thus that all forms of life on this planet are related to one another. The problem of biological time was solved by encoding information in DNA and retrieving the information for each new generation, for it is easier to make a new organism than it is to repair an aging, malfunctioning one. Subsequently, small modi?cations of the standard genetic code were found in certain organisms and in mitochondria. Mitochondrial DNA only encodes about 10–13 proteins, so some modi?cations of the genetic code are tolerated that pr- ably would be lethal if applied to the thousands of kinds of proteins encoded by genomic DNA.