Macrophages have unique and diverse functions necessary for survival. And, in humans (and other species), they are the most abundant leukocytes in tissues. The Innate functions of macrophages that are best known are their unusual ability to either “Kill” or “Repair”. Since killing is a destructive process and repair is a constructive process, it was stupefying how one cell could exhibit these 2 polar – opposite functions. However, in the late 1980’s, it was shown that macrophages have a unique ability to enzymatically metabolize Arginine to Nitric Oxide (NO, a gaseous non – specific killer molecule) or to Ornithine (a precursor of polyamines and collagen for repair). The dual Arginine metabolic capacity of macrophages provided a functional explanation for their ability to kill or repair. Macrophages predominantly producing NO are called M1 and those producing Ornithine are called M2. M1 and M2 – dominant responses occur in lower vertebrates, and in T cell deficient vertebrates being directly driven by Damage and Pathogen Associated Molecular Patterns (DAMP and PAMP). Thus, M1 and M2 are Innate responses that protect the host without Adaptive Immunity. In turn, M1/M2 is supplanting previous models in which T cells were necessary to “activate” or “alternatively activate” macrophages (the Th1/Th2 paradigm). M1 and M2 macrophages were named such because of the additional key findings that these macrophages stimulate Th1 and Th2 – like responses, respectively. So, in addition to their unique ability to kill or repair, macrophages also govern Adaptive Immunity. All of the foregoing would be less important if M1 or M2 – dominant responses were not observed in disease. But, they are. The best example to date is the predominance of M2 macrophages in human tumors where they act like wound repair macrophages and actively promote growth. More generally, humans have become M2 – dominant because sanitation, antibiotics and vaccines have lessened M1 responses. And, M2 dominance seems the cause of ever - increasing allergies in developed countries. Obesity represents a new and different circumstance. Surfeit energy (e.g., lipoproteins) causes monocytes to become M1 dominant in the vessel walls causing plaques. Because M1 or M2 dominant responses are clearly causative in many modern diseases, there is great potential in developing the means to selectively stimulate (or inhibit) either M1 or M2 responses to kill or repair, or to stimulate Th1 or Th2 responses, depending on the circumstance. The contributions here are meant to describe diseases of M1 or M2 dominance, and promising new methodologies to modulate the fungible metabolic machinery of macrophages for better health.

Macrophages are core components of the innate immune system. Once activated, they may have either pro- or anti-inflammatory effects that include pathogen killing, safe disposal of apoptotic cells or tissue renewal. The activation state of macrophages is conceptualized by the so-called M1/M2 model of polarization. M2 macrophages are not simply antagonists of M1 macrophages; rather, they represent a network of tissue resident macrophages with roles in tissue development and organ homeostasis. M2 macrophages govern functions at the interfaces of immunity, tissue development and turnover, metabolism, and endocrine signaling. Dysfunction in M2 macrophages can ruin the healthy interplay between the immune system and metabolic processes, and lead to diseases such as insulin resistance, metabolic syndrome, and type 1 and 2 diabetes mellitus. Furthermore, M2 macrophages are essential for healthy tissue development and immunological self-tolerance. Worryingly, these functions of M2 macrophages can also be disrupted, resulting in tumor growth and autoimmunity. This book comprehensively discusses the biology of M2 macrophages, summarizes the current state of knowledge, and highlights key questions that remain unanswered.

This new edition is a unique combined resource for physicians and scientists addressing the needs of both groups. In addition to stimulating exchange and collaboration and shortening the path between discovery and application of new knowledge, the book helps clinicians understand new therapeutic concepts from their origins. The volume serves as a comprehensive guide to the current diagnostic modalities, including enhanced imaging techniques such as MRI and CT enterography, virtual colonoscopy, ultrasound, and endomicroscopy, as well as conventional and complex immunomodulatory principles. The latest edition also includes revised chapters from the previous edition, as well as new chapters reflecting current developments in the field. Written by experts in their field, Crohn’s Disease and Ulcerative Colitis: From Epidemiology and Immunobiology to a Rational Diagnostic and Therapeutic Approach, Second Edition is of great value to gastroenterologists, surgeons, internists, pediatricians and gynecologists trainees, as well as all those involved in Crohn’s disease, ulcerative colitis, and related autoimmune disorders.

This book deals with the paradoxical role of autophagy in tumor suppression and tumor promotion in cancer cells. Autophagy plays opposing, context-dependent roles in tumors; accordingly, strategies based on inhibiting or stimulating autophagy could offer as potential cancer therapies. The book elucidates the physiological role of autophagy in modulating cancer metastasis, which is the primary cause of cancer-associated mortality. Further, it reviews its role in the differentiation, development, and activation of multiple immune cells, and its potential applications in tumor immunotherapy. In addition, it examines the effect of epigenetic modifications of autophagy-associated genes in regulating tumor growth and therapeutic response and summarizes autophagy’s role in the development of resistance to a variety of anti-cancer drugs in cancer cells. In closing, it assesses autophagy as a potential therapeutic target for cancer treatment. Given its scope, the book offers a valuable asset for all oncologists and researchers who wish to understand the potential role of autophagy in tumor biology.

Bone Pathology is the second edition of the book, A Compendium of Skeletal Pathology that published 10 years ago. Similar to the prior edition, this book complements standard pathology texts and blends new but relatively established information on the molecular biology of the bone. Serving as a bench-side companion to the surgical pathologist, this new edition reflects new advances in our understanding of the molecular biology of bone. New chapters on soft-tissue sarcomas and soft-tissue tumors have been added as well as several additional chapters such as Soft-tissue pathology and Biomechanics. The volume is written by experts who are established in the field of musculoskeletal diseases. Bone Pathology is a combined effort from authors of different specialties including surgeons, pathologists, radiologists and basic scientists all of whom have in common an interest in bone diseases. It will be of great value to surgical pathology residents as well as practicing pathologists, skeletal radiologists, orthopedic surgeons and medical students.

This book combines fundamental concepts of biochemistry and the dental sciences to provide an authentic, coherent and comprehensive text for dental students. It describes in simple language the intricate pathophysiology of biomolecules in health and in diseases of dental and oral tissues. This book also describes the evolution of biochemistry in a chronological order, provides information about the fundamental chemical structure, classification and biological significance of biomolecules, vitamins and hormones, enriched with flow charts and diagrams for easy understanding and quick reference. It includes chapters on nucleic acids, nutrition and serum enzymes and organ function tests, and offers an innovative approach to familiarize dental students with the biochemical composition of enamel, dentine, cementum and saliva, explaining the biochemical basis of dental caries, periodontal diseases, role of fluorides in caries prophylaxis, fluoride toxicity, and the role of amino acids as anti-hypersensitive agents.

This textbook takes you on a journey to the basic concepts of cancer biology. It combines developmental, evolutionary and cell biology perspectives, to then wrap-up with an integrated clinical approach. The book starts with an introductory chapter, looking at cancer in a nut shell. The subsequent chapters are detailed and the idea of cancer as a mass of somatic cells undergoing a micro-evolutionary Darwinian process is explored. Further, the main Hanahan and Weinberg “Hallmarks of Cancer” are revisited. In most chapters, the fundamental experiments that led to key concepts, connecting basic biology and biomedicine are highlighted. In the book’s closing section all of these concepts are integrated in clinical studies, where molecular diagnosis as well as the various classical and modern therapeutic strategies are addressed. The book is written in an easy-to-read language, like a one-on-one conversation between the writer and the reader, without compromising the scientific accuracy. Therefore, this book is suited not only for advanced undergraduates and master students but also for patients or curious lay people looking for a further understanding of this shattering disease