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Rasayanas are non-toxic Ayurvedic complex herbal preparations or individual herbs used to rejuvenate or attain the complete potential of an individual in order to prevent diseases and degenerative changes that leads to disease. The present paper reviews various activities of Rasayanas to support the above concept, its role as a prophylactic medication and significance in the prevention of diseases in both healthy as well as diseased individuals. The emerging data suggest that the possible mechanisms may be by immunostimulation, quenching free radicals, enhancing cellular detoxification mechanisms, repair damaged non-proliferating cells, inducing cell proliferation and self-renewal of damaged proliferating tissues, and replenishing them by eliminating damaged or mutated cells with fresh cells.

A fundamental problem in cancer research is the identification of the cell type capable of initiating and sustaining the growth of the neoplastic clone in vivo. The key to solving this problem lies on the observation made over 40 years ago that tumors are heterogeneous and thus might be maintained only by a rare subset of cells called "cancer stem cells" (CSCs). However, the proof of this principle was only possible after the development of modern research tools for investigating the behavior of defined cell populations in vivo. The blood-related cancer leukemia was the first disease where human CSCs, or leukemic stem cells (LSCs), were isolated. The development of quantitative xenotransplantation assays using immune-deficient mouse recipients to detect primitive human hematopoietic stem cells (HSCs) with in vivo repopulating ability and the adaptation of this model to leukemia have been instrumental. Leukemia can now be viewed as aberrant hematopoietic processes initiated by rare LSCs that have maintained or reacquired the capacity for indefinite proliferation through accumulated mutations and/or epigenetic changes. Yet, despite their critical importance, much remains to be learned about the developmental origin of LSC and the mechanisms responsible for their emergence in the course of the disease. This report will review our current knowledge on normal and leukemic stem cell development and finally demonstrate how these discoveries provide a paradigm for identification of CSCs from solid tumors. By a careful comparative analysis of the properties of CSCs and of their normal counterparts, it should be possible to pinpoint critical features amenable to efficient anti-CSC therapies.

Pluripotent stem (PS) cells have the ability to replicate themselves (self-renew) and to generate virtually any given cell type in the adult body (pluripotency). Human PS (hPS) cells are therefore considered promising sources for future cell replacement therapy. Embryonic stem (ES) cells are the major type of PS cells that are derived from blastocyst embryos. Germ cells from testis can also become PS cells when cultured for a long period with a combination of growth factors. Alternatively, differentiated somatic cells can also be converted to PS cells by the method called nuclear reprogramming. This includes somatic cell nuclear transfer where a somatic cell nucleus is injected into an enucleated oocyte giving rise to a reprogrammed PS cell, as well as the recently developed technique of reprogramming differentiated somatic cells into induced pluripotent stem (iPS) cells by introducing defined transcription factors. Regardless of the sources and generation methods, PS cells share common epithelial structures and maintain tight cellular interactions. Although the molecular mechanisms that regulate self-renewal and pluripotency of PS cells have been extensively studied, the basic cellular interactions that govern how PS cells control cell-cell and cell-matrix adhesions are still not fully understood. In addition, there are several obstacles in the current culture methods for hPS cells that need to be overcome in order to achieve the highest safety and consistency required for clinical applications. A Rho-mediated signaling axis has recently been determined to be the core machinery that integrates cellular interactions between PS cells. By chemically engineering this axis, hPS cells are able to self-renew under completely defined conditions while maintaining their multi-differentiation capacities. When combined with the rapid progress in research focusing on iPS cells, these studies on cell-cell and cell-matrix adhesion in PS cells may not only contribute to further understanding PS cell biology, but also lead to the development of novel technologies enabling the derivation and growth of clinically relevant hPS cells for regenerative therapies.

Stem cells are characterized by their dual ability to self-renew and differentiate, yielding essentially unlimited numbers of progeny that can replenish tissues with either high turnover such as blood and skin or contribute to the regeneration of organs with less frequent remodeling such as muscle. In contrast to their embryonic counterparts, adult stem cells can only preserve their unique functions if they are in intimate contact with an instructive microenvironment, termed niche. Stem cells integrate a complex array of niche signals that regulate their fate, keeping them in a relatively quiescent state during homeostasis, or controlling their numbers via symmetric or asymmetric divisions in response to the regenerative demands of a tissue. This chapter provides an overview of the current state of knowledge of structural and functional hallmarks of mammalian stem cell niches and offers a perspective on how bioengineering principles could be used to deconstruct the niche and providing novel insights into the role of its specific components in the regulation of stem cell fate. Such "artificial niches" constitute powerful tools for elucidating stem cell regulatory mechanisms that should fuel the development of novel therapeutic strategies for tissue regeneration.

A fundamental problem in cancer research is the identification of the cell type capable of initiating and sustaining the growth of the neoplastic clone in vivo. The key to solving this problem lies on the observation made over 40 years ago that tumors are heterogeneous and thus might be maintained only by a rare subset of cells called “cancer stem cells” (CSCs). However, the proof of this principle was only possible after the development of modern research tools for investigating the behavior of defined cell populations in vivo. The blood-related cancer leukemia was the first disease where human CSCs, or leukemic stem cells (LSCs), were isolated. The development of quantitative xenotransplantation assays using immune-deficient mouse recipients to detect primitive human HSCs with in vivo repopulating ability and the adaptation of this model to leukemia has been instrumental. Leukemia can now be viewed as aberrant hematopoietic processes initiated by rare LSCs that have maintained or reacquired the capacity for indefinite proliferation through accumulated mutations and/or epigenetic changes. Yet, despite their critical importance, much remains to be learned about the developmental origin of LSC and the mechanisms responsible for their emergence in the course of the disease. This chapter will review our current knowledge on normal and leukemic stem cell development and finally demonstrate how these discoveries provide a paradigm for identification of cancer stem cell (CSC) from solid tumors.