With the fragile interspecies peace that followed the War With No Name under assault from land and sea, Sheba and Mort(e) have no choice but to take up their arms and enter once again into the conflict that threatened to tear them apart. “Repino's dog, cat, and beaver soldiers are nakedly real, as honest as any characters in modern fiction. As horrible as it may sound, may The War With No Name never end." —Corey Redekop, author of Husk In the aftermath of the War With No Name, the Colony has been defeated, its queen lies dead, and the world left behind will never be the same. In her madness, the queen used a strange technology to uplift the surface animals, turning dogs and cats, bats and bears, pigs and wolves into intelligent, highly evolved creatures who rise up and kill their oppressors. And now, after years of bloodshed, these sentient beasts must learn to live alongside their sworn enemies—humans. Far removed from this newly emerging civilization, a housecat turned war hero named Mort(e) lives a quiet life with the love he thought he had lost, a dog named Sheba. But before long, the chaos that they escaped comes crashing in around them. An unstoppable monster terrorizes a nearby settlement of beavers. A serial killer runs amok in the holy city of Hosanna. An apocalyptic cult threatens the fragile peace. And a mysterious race of amphibious creatures rises from the seas, intent on fulfilling the Colony’s destiny and ridding the world of all humans. No longer able to run away, Sheba and Mort(e) rush headlong into the conflict, ready to fight but unprepared for a world that seems hell-bent on tearing them apart. In the twilight of all life on Earth, love survives, but at a cost that only the desperate and the reckless are willing to pay.

Nathalie Quintane circumvents the biographical to explore this well-known story from inside Joan's experience.

The understanding of chemokines, the proteins that control the migration of cells, and their receptors, is critical to the study of causes and therapies for a wide range of human diseases and infections, including certain types of cancer, inflammatory diseases, HIV, and malaria. This volume, focusing on chemokine structure and function, as well as signaling, and its companion volume (Methods in Enzymology volume 461, focusing on chemokines as potential targets for disease intervention) provide a comprehensive overview and time-tested protocols in this field, making it an essential reference for researchers in the area. - Along with its companion volume, provides a comprehensive overview of chemokine methods, specifically as related to potential disease therapy - Gathers tried, tested, and trusted methods and techniques from top players in chemokine research - Provides an essential reference for researchers in the field

Chemokines are a superfamily of low molecular weight cytokines that were initially described based on their ability to induce the directed migration of leukocytes to sites of inflammation or injury. In humans, there are approximately 45 chemokines that bind to 19 G-protein-coupled receptors. In addition to mediating cellular migration, chemokines have now been shown to affect many cellular functions including survival, adhesion, invasion, proliferation, and to regulate circulating chemokine levels. Although chemokine receptors were first described on leukocytes, it is now appreciated that chemokine receptors are also expressed by many other cells including endothelial and epithelial cells. Since the first description of chemokine receptors on malignant cells in 2001, an extensive literature has developed describing the expression and function of chemokine receptors in many malignancies. These studies support the initial hypothesis that malignant cells use chemokine receptors to migrate to distant sites of ligand expression and that expression of certain receptors is associated with a poor prognosis. It has also become apparent that malignancies of different tissues may use a diverse profile of chemokine receptors and that the same receptor may mediate metastasis to different sites in tumors of different histological origins. Receptor function may also maintain survival and expansion of the primary tumor.

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