Llibres / Capítols de llibre (Biomedicina)

URI permanent per a aquesta col·leccióhttps://hdl.handle.net/2445/174340

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Neuroprotection: A New Therapeutic Approach of Relapsing Remitting Multiple Sclerosis
(IntechOpen, 2016-09-08) Espinosa Parrilla, Juan Francisco; Pugliese, Marco; Mahy Gehenne, Josette Nicole; Rodríguez Allué, Manuel José
Neurodegenerative changes occurring early from primary acute immune-mediated inflammation support the hypothesis that multiple sclerosis (MS) is a complex disease. Axonal loss progresses with the disease course and represents the principal driver of disability. In this context, the pursuit of neuroprotective therapies in multiple sclerosis provides new valid alternatives that could significantly impact on disease progression and neurodegenerative changes, including the promotion of restoration of myelin sheaths through the remyelination process. This chapter reviews promising drugs with proposed neuroprotective or neuroregenerative effects that are currently approved or in clinical trials for the treatment of multiple sclerosis. Although the chapter highlights the diazoxide action on neuroinflammation and the results of a clinical trial with this drug, the review also includes other molecules with oral or parenteral administration.
Don’t Take Away My P: Phosphatases as Therapeutic Targets in Huntington’s Disease
(IntechOpen, 2012-02-15) Saavedra, Ana; Alberch i Vié, Jordi, 1959-; Pérez Navarro, Esther
The molecular bases that account for the preferential neurodegeneration of striatal mediumsized spiny neurons (MSNs) in Huntington’s Disease (HD) are still unknown, and different mechanisms have been proposed to contribute to the neurodegenerative process. These include mitochondrial dysfunction and metabolic impairment, transcriptional dysregulation, altered expression of trophic factors, dopamine toxicity, oxidative stress, and changes in autophagy, and huntingtin (htt) phosphorylation. In addition, excitotoxicity through the overactivation of N-methyl-D-aspartate (NMDA) receptors (NMDARs) has also been proposed to contribute to the preferential loss of these neurons (for review see Ehrnhoefer et al., 2011; Jin & Johnson, 2010; Perez-Navarro et al., 2006; Renna et al., 2010; Rosenstock et al., 2010; Weir et al., 2011). Some of these mechanisms are controlled by the attachment/removal of phosphate groups through the action of protein kinases and protein phosphatases, respectively. Therefore, alterations in their levels/activity in the presence of mutant htt (mhtt) can impact on cell survival...
Cryopreservation of Human Pluripotent Stem Cells: Are We Going in the Right Direction?
(IntechOpen, 2012-03-09) Martín Ibáñez, Raquel; Hovatta, Outi; Canals i Coll, Josep M.
The first derivation of human embryonic stem cells (hESCs) (Thomson et al., 1998) and the more recently development of human induced pluripotent stem cells (iPSCs) (Park et al., 2008; Takahashi et al., 2007; Takahashi & Yamanaka, 2006; Wernig et al., 2007; Yu et al., 2007) have marked the beginning of a new era in biomedical research. These two types of human pluripotent stem cells (hPSCs) are characterized by an unlimited capacity to selfrenew while retaining their potential to differentiate into almost all cell types of the body (Odorico et al., 2001; Reubinoff et al., 2000; Silva & Smith, 2008). These remarkable properties turn hPSCs into one of the most interesting cell types for toxicology and drug discovery, tissue engineering and regenerative medicine (Battey, 2007; Mountford, 2008). In fact, work with hPSCs has already provided new and exciting developments that may eventually lead to the creation of novel cell-based therapies for the treatment of a wide range of human diseases including Parkinson’s and other neurodegenerative diseases, diabetes, cardiac and vascular diseases (Kiskinis & Eggan, 2010; Ronaghi et al., 2010). However, a major challenge for the widespread application of hPSCs is the development of efficient protocols for cryopreservation...
SLAM Family Receptors and Autoimmunity
(IntechOpen, 2011-10-26) Sintes, Jordi; Bastos, Ricardo; Engel Rocamora, Pablo
The immune system is responsible for the defense against a wide array of pathogens but without responding to each individual’s (self) antigens. Autoimmune diseases are characterized by a loss of tolerance to self antigens that leads to the appearance of autoreactive lymphocytes. The main factors that contribute to the development of autoimmunity are genetic susceptibility and infection. Disease susceptibility is the result of the combined action of multiple genes. It has been shown that certain gene polymorphisms can influence the establishment of self-tolerance. The human immune system is a complex machinery involving numerous proteins. Cell-surface proteins expressed by leukocytes are of particular relevance due not only to their participation in the network of interactions that regulate the innate and adaptive immune responses, but also to their potential as excellent targets for diagnostic and therapeutic interventions (Diaz-Ramos et al., 2011). These molecules deliver signals that modulate leukocyte development, activation, survival, clonal expansion, and important effector functions. Some of these cell-surface signaling molecules have the capacity to activate lymphocytes and other leukocytes, while others function as downmodulators of immune responses, playing a key role in the establishment of tolerance to self antigens. Thus, it is not surprising that many of the allelic variants associated with autoimmunity identified, to date, correspond to leukocyte cell-surface molecules (Maier & Hafler, 2009). In this review we will discuss recent observations that point to a key role of signaling lymphocyte activation molecule family (SLAMF) receptors in the development of autoimmunity.

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