Search Results for cellular

... of signaling that is important for specific types of cellular responses. OXRs are able to form complexes with several other G-protein-coupled receptors in vitro, and one possibility is that the complexing partners regulate the use of certain signal transducers. In the central nervous system neurons, the main...

... Abstract Low energy extracorporeal shockwave (SW) therapy (ESWT) has been used to improve blood flow recovery and reduce inflammation in muscle and organs with ischemia/reperfusion injury. In recent decades, through cultured cell models and experimental animal studies, several intra-cellular...

... in their main activity, with decreased cytotoxic activity on the single-cell level potentially compensated for by increased NK cell numbers. Interestingly, some parameters such as the expression of CD16 and the antibody-dependent cellular cytotoxicity capacity are not dependent on age. The reasons...

.... Induction of donor-specific tolerance to eliminate the requirement of immunosuppression has thus become an ultimate goal that is actively pursued in the field of transplantation. Among the various strategies, great potential has been shown with cellular therapeutics in many animal studies. This chapter...

... such as prostaglandins, interleukins, chemokines, leukotrienes, growth factors, wnt signalling and bone morphogenetic proteins are involved in the regulation of bone remodeling. We discuss here cells and mediators involved in the cellular and molecular machanisms of bone resorption and bone formation. Cell Types...

... that cellular senescence is an underlying mechanism of aging and age-related conditions. Cellular senescence is a process in which cells lose the ability to divide and damage neighboring cells by the factors they secrete, collectively referred to as the senescence-associated secretory phenotype (SASP). Herein...

.... This evidence seems to reflect that aging itself can be understood as the accumulation of deficits from subcellular processes to tissues to organs that manifest as clinical changes [ 3 ]. As a consequence, a further argument that unites aging, deficit accumulation and frailty is that cellular and molecular...

... studies or, ultimately, be approved as licensed cellular therapeutics. Here, we describe the principles behind the manufacturing of clinical-grade cellular products, as well as potential methods for large-scale expansion and processing according to Good Manufacturing Practice (GMP) standards sets...

... on membrane composition and consequently on membrane function and cellular responses, with emphasis on the high variability of responses within the human race. While environmental factors have been recognized to be at the origin of some variability, recent studies have clarified the decisive role of genetics...

... individual susceptibility. In some individuals and with some bacteria this will be an innate-only response, others will need to invoke the inflammatory response, and yet others will require the adaptive immune response – be it cellular, humoral or both – to reduce or remove the challenge from the microbes...

... or deletions in the ephrin-B1 encoding gene EFNB1 located at Xq12/13. The transmembrane protein ephrin-B1 is a regulator of cell-cell communication involved in diverse cellular functions such as axon guidance, and cell sorting and migration, which best explains the peculiar appearance of CFNS as reflecting...

... cellular and molecular mechanisms underlying age related bone loss. This chapter focuses on the current concepts and paradigms of age related bone loss in humans and how various animal and cellular models have broadened our understanding in this fascinating but complex area. Changes in hormonal, neuronal...

... but also specificity in the action of TNF. The inherent complexity in TNF-mediated pathophysiology highlights the requirement to address the role of TNF taking into account both proinflammatory tissue-damaging and immunomodulatory functions in a cellular and receptor-specific manner. In this review, we...