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“Bracingly intelligent, lucid, balanced—witty, too.... A scrupulous and charming look at our modern understanding of genes and experience.” — Oliver SacksArmed with extraordinary new discoveries about our genes, acclaimed science writer Matt Ridley turns his attention to the nature-versus-nurture debate in a thoughtful book about the roots of human behavior.Ridley recounts the hundred years'war between the partisans of nature and nurture to explain how this paradoxical creature, the human being, can be simultaneously free-willed and motivated by instinct and culture. With the decoding of the human genome, we now know that genes not only predetermine the broad structure of the brain, they also absorb formative experiences, react to social cues, and even run memory. They are consequences as well as causes of the will.

Approximately three percent of newborn humans have congenital anomalies with significant cosmetic and/or functional consequences. Much of our ability to understand what has gone awry in these birth defects rests with development of animal models for them; the mouse has emerged as the model organism of choice for these studies. This volume reviews mouse models of specific developmental genetic diseases, including neural tube defects; cleft lip and/or palate; congenital heart disease; ciliopathies; hereditary deafness and others to provide conceptual insight into congenital anomalies generally. The interplay between clinical observation and murine model systems is expected to yield deep insight into mammalian developmental processes and the emergence of effective preventive and/or therapeutic strategies. - Provides busy clinical and basic science researchers a one-stop overview and synthesis of the latest research findings and contemporary thought in the area - Allows researchers to compare and contrast disease models and also to learn about what models have been developed for large-scale distribution - Allows researchers to evaluate basic differences in mouse and human biology and propose alternate pathways and possible gene interactions of the disease