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In April 1909, two waves of massacres shook the province of Adana, located in the southern Anatolia region of modern-day Turkey, killing more than 20,000 Armenians and 2,000 Muslims. The central Ottoman government failed to prosecute the main culprits, a miscarriage of justice that would have repercussions for years to come. Despite the significance of these events and the extent of violence and destruction, the Adana Massacres are often left out of historical narratives. The Horrors of Adana offers one of the first close examinations of these events, analyzing sociopolitical and economic transformations that culminated in a cataclysm of violence. Bedross Der Matossian provides voice and agency to all involved in the massacres—perpetrators, victims, and bystanders. Drawing on primary sources in a dozen languages, he develops an interdisciplinary approach to understand the rumors and emotions, public spheres and humanitarian interventions that together informed this complex event. Ultimately, through consideration of the Adana Massacres in micro-historical detail, this book offers an important macrocosmic understanding of ethnic violence, illuminating how and why ordinary people can become perpetrators.

\"In this book, William Kelleher Storey shows that guns and discussions about guns during the 17th, 18th, and 19th centuries were fundamentally important to the establishment of racial discrimination in South Africa. Relying mainly on materials held in archives and libraries in Britain and South Africa, Storey explains the workings of the gun trade and the technological development of the firearms. He relates the history of firearms to ecological, political, and social changes, showing that there is a close relationship between technology and politics in South Africa.\"--BOOK JACKET.

Key Points NF-κB (nuclear factor-κB) activation is mediated by two main signalling pathways, the canonical and non-canonical pathways, which differ in both signalling mechanisms and biological functions. The canonical NF-κB pathway is stimulated by ligands of diverse immune receptors and involves the rapid and transient activation of IκB kinase (IKK), IKK-mediated IκBα phosphorylation, and subsequent IκBα degradation and nuclear translocation of canonical NF-κB members, including p50, RELA and c-REL. The non-canonical NF-κB pathway selectively responds to signals from a subset of tumour necrosis factor receptor (TNFR) superfamily members and involves slow and persistent activation of NF-κB-inducing kinase (NIK), NIK-mediated p100 phosphorylation, and subsequent p100 processing and nuclear translocation of non-canonical NF-κB members, including p52 and RELB. The non-canonical NF-κB pathway is tightly controlled by ubiquitin-dependent degradation of NIK mediated by an E3 ubiquitin ligase complex composed of cIAP family members, TNFR-associated factor 2 (TRAF2) and TRAF3; activation of non-canonical NF-κB involves signal-induced disruption of the cIAP E3 complex, typically via degradation of TRAF3, and accumulation of NIK. The non-canonical NF-κB pathway regulates important aspects of immune functions, including lymphoid organ development, the cross-priming function of dendritic cells, B cell survival and germinal centre reactions, generation and maintenance of effector and memory T cells, and antiviral innate immunity. The non-canonical NF-κB pathway is involved in various inflammatory diseases, such as rheumatoid arthritis, systemic lupus erythematosus, kidney inflammation and injury, metabolic inflammation, and central nervous system inflammation. Defects in the non-canonical pathway of NF-κB activation are associated with severe immune deficiencies, and aberrant activation of this pathway can cause autoimmune and inflammatory diseases. Here, the author investigates the activation, signalling mechanisms and the biological function of the non-canonical NF-κB pathway. The nuclear factor-κB (NF-κB) family of transcription factors is activated by canonical and non-canonical signalling pathways, which differ in both signalling components and biological functions. Recent studies have revealed important roles for the non-canonical NF-κB pathway in regulating different aspects of immune functions. Defects in non-canonical NF-κB signalling are associated with severe immune deficiencies, whereas dysregulated activation of this pathway contributes to the pathogenesis of various autoimmune and inflammatory diseases. Here we review the signalling mechanisms and the biological function of the non-canonical NF-κB pathway. We also discuss recent progress in elucidating the molecular mechanisms regulating non-canonical NF-κB pathway activation, which may provide new opportunities for therapeutic strategies.

The break-up of the Ottoman empire and the disintegration of the Russian empire were watershed events in modern history. The unravelling of these empires was both cause and consequence of World War I and resulted in the deaths of millions. It irrevocably changed the landscape of the Middle East and Eurasia and reverberates to this day in conflicts throughout the Caucasus and Middle East. Shattering Empires draws on extensive research in the Ottoman and Russian archives to tell the story of the rivalry and collapse of two great empires. Overturning accounts that portray their clash as one of conflicting nationalisms, this pioneering study argues that geopolitical competition and the emergence of a new global interstate order provide the key to understanding the course of history in the Ottoman-Russian borderlands in the twentieth century. It will appeal to those interested in Middle Eastern, Russian, and Eurasian history, international relations, ethnic conflict, and World War I.

How glutamine metabolism orchestrates macrophage activation is unclear. Ho and colleagues show glutamine metabolism tailors the immune responses of macrophages through metabolic and epigenetic reprogramming. Glutamine metabolism provides synergistic support for macrophage activation and elicitation of desirable immune responses; however, the underlying mechanisms regulated by glutamine metabolism to orchestrate macrophage activation remain unclear. Here we show that the production of α-ketoglutarate (αKG) via glutaminolysis is important for alternative (M2) activation of macrophages, including engagement of fatty acid oxidation (FAO) and Jmjd3-dependent epigenetic reprogramming of M2 genes. This M2-promoting mechanism is further modulated by a high αKG/succinate ratio, whereas a low ratio strengthens the proinflammatory phenotype in classically activated (M1) macrophages. As such, αKG contributes to endotoxin tolerance after M1 activation. This study reveals new mechanistic regulations by which glutamine metabolism tailors the immune responses of macrophages through metabolic and epigenetic reprogramming.

Inflammation is a fundamental protective response that sometimes goes awry and becomes a major cofactor in the pathogenesis of many chronic human diseases, including cancer. Here we review the evolutionary relationship and opposing functions of the transcription factor NF-κB in inflammation and cancer. Although it seems to fulfill a distinctly tumor-promoting role in many types of cancer, NF-κB has a confounding role in certain tumors. Understanding the activity and function of NF-κB in the context of tumorigenesis is critical for its successful taming, an important challenge for modern cancer biology.

NF-κB proteins are a family of transcription factors that are of central importance in inflammation and immunity. NF-κB also plays important roles in other processes, including development, cell growth and survival, and proliferation, and is involved in many pathological conditions. Reactive Oxygen Species (ROS) are created by a variety of cellular processes as part of cellular signaling events. While certain NF-κB-regulated genes play a major role in regulating the amount of ROS in the cell, ROS have various inhibitory or stimulatory roles in NF-κB signaling. Here we review the regulation of ROS levels by NF-κB targets and various ways in which ROS have been proposed to impact NF-κB signaling pathways.

NF-κB transcription factors are critical regulators of immunity, stress responses, apoptosis and differentiation. A variety of stimuli coalesce on NF-κB activation, which can in turn mediate varied transcriptional programs. Consequently, NF-κB-dependent transcription is not only tightly controlled by positive and negative regulatory mechanisms but also closely coordinated with other signaling pathways. This intricate crosstalk is crucial to shaping the diverse biological functions of NF-κB into cell type– and context-specific responses.