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What does it mean to cross half a continent without documents or rights? The self-told story of African migration.

This book is a record of the Black music culture that emerged in post-colonial London at the end of the twentieth century; the people who made it, the racial and spatial politics of its development and change, and the part it played in founding London's precious, embattled multiculture. It tells the story of the linked Black musical scenes of the city, from ska, reggae and soul in the 1970s, to rare groove and rave in the 1980s and jungle and its offshoots in the 1990s, to dubstep and grime of the 2000s. Melville argues that these demonstrate enough common features to be thought of as one musical culture, an Afro-diasporic continuum. Core to this idea is that this dance culture has been ignored in history and cultural theory and that it should be thought of as a powerful and internationally significant form of popular art.This book is a record of the Black music culture that emerged in post-colonial London at the end of the twentieth century; the people who made it, the racial and spatial politics of its development and change, and the part it played in founding London's precious, embattled multiculture. It tells the story of the linked Black musical scenes of the city, from ska, reggae and soul in the 1970s, to rare groove and rave in the 1980s and jungle and its offshoots in the 1990s, to dubstep and grime of the 2000s. Melville argues that these demonstrate enough common features to be thought of as one musical culture, an Afro-diasporic continuum. Core to this idea is that this dance culture has been ignored in history and cultural theory and that it should be thought of as a powerful and internationally significant form of popular art.

Black Legacies looks at color-based prejudice in medieval and modern texts in order to reveal key similarities. Bringing far-removed time periods into startling conversation, this book argues that certain attitudes and practices present in Europe's Middle Ages were foundational in the development of the western concept of race. Using historical, literary, and artistic sources, Lynn Ramey shows that twelfth- and thirteenth-century discourse was preoccupied with skin color and the coding of black as \"evil\" and white as \"good.\" Ramey demonstrates that fears of miscegenation show up in all medieval European societies. She pinpoints these same ideas in the rhetoric of later centuries. Mapmakers and travel writers of the colonial era used medieval lore of \"monstrous peoples\" to question the humanity of indigenous New World populations, and medieval arguments about humanness were employed to justify the slave trade. Ramey even analyzes how race is explored in films set in medieval Europe, revealing an enduring fascination with the Middle Ages as a touchstone for processing and coping with racial conflict in the West today.

It would be easy to assume that, in the eighteenth century, slavery and the culture of taste--the world of politeness, manners, and aesthetics--existed as separate and unequal domains, unrelated in the spheres of social life. But to the contrary,Slavery and the Culture of Tastedemonstrates that these two areas of modernity were surprisingly entwined. Ranging across Britain, the antebellum South, and the West Indies, and examining vast archives, including portraits, period paintings, personal narratives, and diaries, Simon Gikandi illustrates how the violence and ugliness of enslavement actually shaped theories of taste, notions of beauty, and practices of high culture, and how slavery's impurity informed and haunted the rarified customs of the time. Gikandi focuses on the ways that the enslavement of Africans and the profits derived from this exploitation enabled the moment of taste in European--mainly British--life, leading to a transformation of bourgeois ideas regarding freedom and selfhood. He explores how these connections played out in the immense fortunes made in the West Indies sugar colonies, supporting the lavish lives of English barons and altering the ideals that defined middle-class subjects. Discussing how the ownership of slaves turned the American planter class into a new aristocracy, Gikandi engages with the slaves' own response to the strange interplay of modern notions of freedom and the realities of bondage, and he emphasizes the aesthetic and cultural processes developed by slaves to create spaces of freedom outside the regimen of enforced labor and truncated leisure. Through a close look at the eighteenth century's many remarkable documents and artworks,Slavery and the Culture of Tastesets forth the tensions and contradictions entangling a brutal practice and the distinctions of civility.

Resequencing of genes from individuals of European and African American ancestry indicates that approximately 73% of all protein-coding SNVs and approximately 86% of SNVs predicted to be deleterious arose in the past 5,000–10,000 years, and that European Americans carry an excess of deleterious variants in essential and Mendelian disease genes compared to African Americans. Recent genetic change in a human population As part of the NHLBI Exome Sequencing Project, the exomes of more than 6,500 individuals of European American and African American ancestry have been sequenced. Using these data, the authors estimate that about 73% of all protein-coding single nucleotide variants (SNVs) and 86% of SNVs predicted to be deleterious arose in the past 5,000–10,000 years, a short span in evolutionary time that coincides with a period of accelerated population growth. Around 86% of changes predicted to be harmful arose within the same timeframe, with European Americans harbouring more harmful variants in essential and Mendelian disease genes than African Americans. The data suggest that the increased mutational capacity of recent human populations has influenced the burden of Mendelian disorders, but is also likely to promote beneficial genetic changes that will be selected in future generations to come. More practically, the results will be of use in prioritizing potential disease-causing variants in gene-mapping studies. Establishing the age of each mutation segregating in contemporary human populations is important to fully understand our evolutionary history 1 , 2 and will help to facilitate the development of new approaches for disease-gene discovery 3 . Large-scale surveys of human genetic variation have reported signatures of recent explosive population growth 4 , 5 , 6 , notable for an excess of rare genetic variants, suggesting that many mutations arose recently. To more quantitatively assess the distribution of mutation ages, we resequenced 15,336 genes in 6,515 individuals of European American and African American ancestry and inferred the age of 1,146,401 autosomal single nucleotide variants (SNVs). We estimate that approximately 73% of all protein-coding SNVs and approximately 86% of SNVs predicted to be deleterious arose in the past 5,000–10,000 years. The average age of deleterious SNVs varied significantly across molecular pathways, and disease genes contained a significantly higher proportion of recently arisen deleterious SNVs than other genes. Furthermore, European Americans had an excess of deleterious variants in essential and Mendelian disease genes compared to African Americans, consistent with weaker purifying selection due to the Out-of-Africa dispersal. Our results better delimit the historical details of human protein-coding variation, show the profound effect of recent human history on the burden of deleterious SNVs segregating in contemporary populations, and provide important practical information that can be used to prioritize variants in disease-gene discovery.

Whole-exome sequencing reveals that a rare variant of phospholipase D3 ( PLD3 ( V232M )) segregates with Alzheimer’s disease status in two independent families and doubles risk for the disease in case–control series, and that several other PLD3 variants increase risk for Alzheimer’s disease in African Americans and people of European descent. New genetic risk variant for Alzheimer's disease The identification of mutations causing Alzheimer's disease in amyloid-β precursor protein, presenilin 1 and presenilin 2 led to a better understanding of the pathobiology of the condition. Further mutations are expected to be implicated, but the identification of such variants has been challenging. These authors used exome sequencing to identify low-frequency coding variants with large effects on late-onset Alzheimer's disease. They report several coding variants in the gene PLD3 , coding for phospholipase D3, that increase disease risk at least twofold. PLD3 may have a role in the processing of amyloid-β and may have potential as a novel therapeutic target. Genome-wide association studies (GWAS) have identified several risk variants for late-onset Alzheimer's disease (LOAD) 1 , 2 . These common variants have replicable but small effects on LOAD risk and generally do not have obvious functional effects. Low-frequency coding variants, not detected by GWAS, are predicted to include functional variants with larger effects on risk. To identify low-frequency coding variants with large effects on LOAD risk, we carried out whole-exome sequencing (WES) in 14 large LOAD families and follow-up analyses of the candidate variants in several large LOAD case–control data sets. A rare variant in PLD3 (phospholipase D3; Val232Met) segregated with disease status in two independent families and doubled risk for Alzheimer’s disease in seven independent case–control series with a total of more than 11,000 cases and controls of European descent. Gene-based burden analyses in 4,387 cases and controls of European descent and 302 African American cases and controls, with complete sequence data for PLD3 , reveal that several variants in this gene increase risk for Alzheimer’s disease in both populations. PLD3 is highly expressed in brain regions that are vulnerable to Alzheimer’s disease pathology, including hippocampus and cortex, and is expressed at significantly lower levels in neurons from Alzheimer’s disease brains compared to control brains. Overexpression of PLD3 leads to a significant decrease in intracellular amyloid-β precursor protein (APP) and extracellular Aβ42 and Aβ40 (the 42- and 40-residue isoforms of the amyloid-β peptide), and knockdown of PLD3 leads to a significant increase in extracellular Aβ42 and Aβ40. Together, our genetic and functional data indicate that carriers of PLD3 coding variants have a twofold increased risk for LOAD and that PLD3 influences APP processing. This study provides an example of how densely affected families may help to identify rare variants with large effects on risk for disease or other complex traits.

There was immense social and economic upheaval between the Black Death and the English Reformation, and contemporary writers often blamed this upheaval on immorality, singling out women's behavior for particular censure. Late medieval moral treatises and sermons increasingly connected good behavior for women with Christianity, and their failure to conform to sin. Katherine L. French argues, however, that medieval laywomen both coped with the chaotic changes following the plague and justified their own changing behavior by participating in local religion. Through active engagement in the parish church, the basic unit of public worship, women promoted and validated their own interests and responsibilities.Scholarship on medieval women's religious experiences has focused primarily on elite women, nuns, and mystics who either were literate enough to leave written records of their religious ideas and behavior or had access to literate men who did this for them. Most women, however, were not literate, were not members of religious orders, and did not have private confessors. As The Good Women of the Parish shows, the great majority of women practiced their religion in a parish church. By looking at women's contributions to parish maintenance, the ways they shaped the liturgy and church seating arrangements, and their increasing opportunities for collective action in all-women's groups, the book argues that gendered behavior was central to parish life and that women's parish activities gave them increasing visibility and even, on occasion, authority. In the face of demands for silence, modesty, and passivity, women of every social status used religious practices as an important source of self-expression, creativity, and agency.

Individual responses to hepatitis C virus Hepatitis C is one of the most common infections in the world. Many of its estimated 170 million sufferers live with the disease for years with no serious symptoms, but in about one in four patients it leads to cirrhosis of the liver. The discovery of a biomarker that predicts an individual's response to hepatitis C treatment raises the possibility that clinical outcomes could be improved by raising patient compliance to the often demanding interferon treatment regime. The new marker is a 'single letter' genetic variant — a C (cytosine) replacing a T (thymidine) in a segment of DNA near the IL28B gene that encodes interleukin 28B (interferon-γ-3). This finding goes some way towards explaining the different treatment outcomes between individuals of European (high IL28B frequency), African and Asian ancestry. And importantly, it is of immediate clinical utility. 170 million people worldwide are chronically infected with hepatitis C virus (HCV), which is the leading cause of cirrhosis in North America. Many patients are not cured by the current recommended treatment regime, with patients of European ancestry having a higher probability of being cured than those of African ancestry. Here, a genetic polymorphism near the IL28B gene is found to be associated with a better response to treatment; it occurs with higher frequency in European populations. Chronic infection with hepatitis C virus (HCV) affects 170 million people worldwide and is the leading cause of cirrhosis in North America 1 . Although the recommended treatment for chronic infection involves a 48-week course of peginterferon-α-2b (PegIFN-α-2b) or -α-2a (PegIFN-α-2a) combined with ribavirin (RBV), it is well known that many patients will not be cured by treatment, and that patients of European ancestry have a significantly higher probability of being cured than patients of African ancestry. In addition to limited efficacy, treatment is often poorly tolerated because of side effects that prevent some patients from completing therapy. For these reasons, identification of the determinants of response to treatment is a high priority. Here we report that a genetic polymorphism near the IL28B gene, encoding interferon-λ-3 (IFN-λ-3), is associated with an approximately twofold change in response to treatment, both among patients of European ancestry ( P = 1.06 × 10 -25 ) and African-Americans ( P = 2.06 × 10 -3 ). Because the genotype leading to better response is in substantially greater frequency in European than African populations, this genetic polymorphism also explains approximately half of the difference in response rates between African-Americans and patients of European ancestry.