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The new microfinance handbook provides a primer on financial services for the poor. It is written for a wide audience, including practitioners, facilitators, policy makers, regulators, investors, and donors working to improve the financial system, but who are relatively new to the sector. It will also be useful for telecommunication companies and other support service providers, students and academics, and consultants and trainers. Although this book is in part an update of the original handbook, the growth of the sector and the complexity of the financial market system have led to a perspective much broader than the previous 'financial and institutional perspective.' As a result, additional chapters have been added to address issues more relevant than when the original handbook was written. To reflect this complexity, the author invited a number of experts to write many of the new chapters. In addition, given that this book does not go into as much detail as the previous book did, a list of key resources at the end of each chapter provides readers additional information on specific topics. Finally, although the title still uses the term microfinance, the book very much addresses the wider financial ecosystem, moving beyond the traditional meaning of microfinance to inclusive financial systems.

Complement component C5 is crucial for experimental animal inflammatory tissue damage; however, its involvement in human inflammation is incompletely understood. The responses to Gram-negative bacteria were here studied taking advantage of human genetic complement-deficiencies--nature's own knockouts--including a previously undescribed C5 defect. Such deficiencies provide a unique tool for investigating the biological role of proteins. The experimental conditions allowed cross-talk between the different inflammatory pathways using a whole blood model based on the anticoagulant lepirudin, which does not interfere with the complement system. Expression of tissue factor, cell adhesion molecules, and oxidative burst depended highly on C5, mediated through the activation product C5a, whereas granulocyte enzyme release relied mainly on C3 and was C5a-independent. Release of cytokines and chemokines was mediated to varying degrees by complement and CD14; for example, interleukin (IL)-1β and IL-8 were more dependent on complement than IFN-γ and IL-6, which were highly dependent on CD14. IL-1 receptor antagonist (IL-1ra) and IFN-γ inducible protein 10 (IP-10) were fully dependent on CD14 and inversely regulated by complement, that is, complement deficiency and complement inhibition enhanced their release. Granulocyte responses were mainly complement-dependent, whereas monocyte responses were more dependent on CD14. Notably, all responses were abolished by combined neutralization of complement and CD14. The present study provides important insight into the comprehensive role of complement in human inflammatory responses to Gram-negative bacteria.