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Llibres / Capítols de llibre (Ciències Fisiològiques)

URI permanent per a aquesta col·leccióhttps://hdl.handle.net/2445/21662

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  • logoOpenAccessPart del llibre
    Embryonic Neural Stem Cell Differentiation to Aldynoglia Induced by Olfactory Bulb Ensheathing Cell-Conditioned Medium
    (IntechOpen, 2011-04-26) Ortuño Sahagún, Daniel; Rojas-Mayorquín, Argelia E.; Camins Espuny, Antoni; Pallàs i Llibería, Mercè, 1964-
    Although the relevance of glial cells in regulating brain activity was predicted by Ramon y Cajal more than a century ago (García-Marín et al., 2007), it was not until almost fifty years ago that initial descriptions of a close functional relationship between neuroglia and neuronal perikarya (Hyden, 1962) or axonal processes (Blunt et al, 1965) began to reveal that neurons and glial cells operate as functional units in the central nervous system (CNS). However, this functional interaction has only been more carefully studied and analysed in the last few decades, generating a substantial increase in research on the roles of neuron– glia interactions in the control of brain function. Glial cells have subsequently been implicated in many functions, including: guiding the migration of neurons in early development, axonal guidance and being responsible for their integrity, forming the necessary scaffold for neuronal architecture and neural protection and proliferation by trophic effects, modulating neurodegenerative processes, and also being critical participants in synaptic transmission, and key regulators of neurotransmitter release...
  • logoOpenAccessPart del llibre
    Liver Glucokinase and Lipid Metabolism
    (IntechOpen, 2012-02-03) Vidal Alabró, Anna; Méndez-Lucas, Andrés; Semakova, Jana; Gómez-Valadés, Alícia G.; Perales Losa, Carlos
    Control of energy metabolism is crucial for optimal functioning of organs and tissues. Amongst all nutrients, glucose is the principal energy source for most cells and, therefore, minimum blood glucose levels must be guaranteed. Alterations in glycaemia can lead to hyperglycaemic states (producing protein glycosylation and toxicity in glucose-sensitive cells) or hypoglycaemic states (that can affect brain function), both harmful. Therefore, mechanisms must exist to keep glycaemia in a narrow physiological range (4-8 mM) independently of the nutritional state. To achieve control of blood glucose levels, our body has a complex, interorgan signaling system using nutrients (glucose, lipids, amino acids), hormones (insulin, glucagon, ghrelin, etc.) and the autonomic nervous system. In response to these signals, organs and tissues (mainly intestine, endocrine pancreas, liver, skeletal muscle, adipose tissue, brain and adrenal glands) adapt their function to energetic requirements. The liver plays a pivotal role in the maintenance of glucose homeostasis by continuously adapting its metabolism to energetic needs. In the fed state, when blood glucose levels are high and there is insulin, liver takes-up part glucose to replenish glycogen stores. Besides, when glucose stores are full, the liver has the capacity to synthesize lipids de novo from glucose for-long term energy storage. Lipids are packaged in very low-density lipoprotein (VLDL) particles and then transported to the adipose tissue. Conversely during starvation, when glycaemia falls and glucagon increases, the liver produces glucose to maintain circulating glucose levels by breaking down glycogen stores or by synthesizing glucose de novo through gluconeogenesis. Gluconeogenesis, as an energy-consuming pathway, is linked to 􀇃-oxidation of fatty acids (fuel supplier pathway)...
  • logoOpenAccessPart del llibre
    Molecular Mechanisms of Acute Brain Injury and Ensuing Neurodegeneration
    (InTech, 2012-03) Ortega González, Fco. Javier; Vidal Taboada, José Manuel; Mahy Gehenne, Josette Nicole; Rodríguez Allué, Manuel José
    Injury to the central nervous system (CNS), including stroke, traumatic brain injury and spinal cord injury, cause devastating and irreversible damage and loss of function. For example, stroke affects very large patient populations, results in major suffering for the patients and their relatives, and involves a significant cost to society. CNS damage implies disruption of the intricate internal circuits involved in cognition, the sensory-motor functions, and other important functions. There are currently no treatments available to properly restore such lost functions. New therapeutic proposals will emerge from an understanding of the interdependence of molecular and cellular responses to CNS injury, in particular the inhibitory mechanisms that block regeneration and those that enhance neuronal plasticity...
  • logoOpenAccessPart del llibre
    Microglia, Calcification and Neurodegenerative Diseases
    (InTech, 2011-12) Vidal Taboada, José Manuel; Mahy Gehenne, Josette Nicole; Rodríguez Allué, Manuel José
    Neurodegeneration is a complex process involving different cell types and neurotransmitters. A common characteristic of neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, Huntington’s disease (HD) and Amyotrophic Lateral Sclerosis (ALS) is the occurrence of a neuroinflammatory reaction in which cellular processes involving glial cells (mainly microglia and astrocytes) and T cells are activated in response to neuronal death. This inflammatory reaction has recently received attention as an unexpected potential target for the treatment of these diseases. Microglial cells have a mesenchymal origin, invade the central nervous system (CNS) prenatally (Chan et al., 2007b) and are the resident macrophages in the CNS (Ransohoff & Perry, 2009). They comprise approximately 10-20% of adult glia and serve as the CNS innate immune system. In neurodegenerative diseases, microglia is activated by misfolded proteins. In the case of AD, amyloid-􀇃 (A􀇃) peptides accumulate extracellularly and activate the microglia locally. In the case of PD, ALS and HD, the misfolded proteins accumulate intracellularly but are still associated with activation of the microglia (Perry et al., 2010). Reactive microglia in the substantia nigra and striatum of PD brains have been described, and increased levels of proinflammatory cytokines and inducible nitric oxide synthase have been detected in these brain regions, providing evidence of a local inflammatory reaction (Hirsch & Hunot, 2009). The injection of lipopolysaccharide (a potent microglia activator) into the substantia nigra produces microglial activation and the death of dopaminergic cells. These findings support the hypothesis that microglial activation and neuroinflammation contribute to PD pathogenesis (Herrera et al., 2000)...
  • logoOpenAccessPart del llibre
    Advances in medical imaging applied to bone metastases
    (InTech, 2011-12) González Sistal, Ángel; Baltasar Sánchez, Alicia; Herranz Carnero, Michel; Ruibal Morell, Álvaro
    Bone metastases are the result of a primary cancer invasion which spreads into the bone marrow through the lymphogenous or hematogenous pathways. Bone metastases are a common complication of cancer.The primary cancers that most frequently metastasize to bone are breast and prostate cancer (65 - 75 %) amongst many others (thyroid 42 %, lung 36 % or kidney 35 %) (Suva et al., 2011). Although the exact incidence of bone metastases is unknown given its dependence on the type of primary cancer, it is estimated that 350,000 people die of bone metastases annually in the United States.