Books published by Nova Science Publishers Inc

Each species has its own characteristic aging trajectory coded by a species-specific developmental program. This developmental program is triggered at the time of fertilization, hence aging begins at conception. Within a species there are considerable variations in the aging phenotype between individuals due to the plasticity of the developmental process and its inherent stochasticity. The evolution of a species is due to genetic changes in its underlying developmental program and when enough genetic changes have accumulated a new species emerges with its own characteristic aging phenotype. Therefore, speciation and aging are linked processes. Over the evolutionary course of the human lineage, culture has been an important driver of evolutionary change. Culture is not restricted to the human lineage but only humans have evolved cumulative culture; the transmission of modified cultural practices across generations. Early cultural innovations such as toolmaking, agriculture and dairy farming had a utilitarian function. However, over the past 100 to 150 years, there has been a significant change in the pace and nature of cultural innovations. Although many cultural innovations still have a utilitarian function, a new category of cultural innovations has emerged that have "entertainment" functions in the domains of social communication and information transfer. In addition, cultural practices by the tobacco, food and technological industries have been used to modify population behaviors, physiology and beliefs. Over the past 50 to 75 years, there has emerged so called chronic non-infectious diseases, which occurrence parallels the development of these new cultural innovations and practices. In addition, culture has now become the primary driver of human evolution. In answer to the question posed by the title of this book, aging is not a disease and diseases are cultural constructs used to define variants in the aging process.

Inflammatory markers, oncogenes, tumor suppressor genes and cell cycle regulators in skin growths represent a series of reports and reviews on skin cancers and precancers, their host immune responses and correlations with medical literature data. We were able to clearly identify an immune response in multiple skin cancers, as well as in cutaneous pre-cancerous conditions. In poorly differentiated tumor areas, some classic immunohistochemical stains did not stain as frequently described in the literature. Other important phenomena we observed are that many cell cycle regulators, cell cycle checkpoints, oncogenes and tumor suppressor gene markers were not only positive inside the tumors, but also in cells around the tumor. Portions of adjacent skin appendices and in supposedly normal adjacent epidermal and dermal tissue also showed signs of these components. These common findings raised questions concerning marginal definition of cutaneous surgery; that is, many of the immunologic findings could not be correlated on classical hematoxylin and eosin reviews. We also noted that many immunologic cells around skin cancers and/or pre-cancers showed high rates of division defined via markers such as Ki-67; our findings utilizing double color immunohistochemistry also showed that these immune cells are possibly actively duplicating as effector cells. Ki-67 has been cited as a superb proliferation marker in melanoma, but additional review of its utility is warranted given our results. Finally, we also found double staining immunohistochemistry to be of excellent value in detecting melanoma cells metastasizing in blood vessels, lymphatics and/or nerves.