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Libros sobre el tema "Reticular stress"

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Autor: Grafiati
Publicado: 15 de junio de 2024

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1

Agostinis, Patrizia y Samali Afshin, eds. Endoplasmic Reticulum Stress in Health and Disease. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4351-9.

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2

illustrator, Kelly Ryan 1976, Lapham David illustrator, Colak Mirko 1975 illustrator y Mutti Andrea 1973 illustrator, eds. Saucer Country: The Reticulan Candidate. New York: DC Comics, 2013.

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3

The unfolded protein response und cellular stress. Amsterdam [etc.]: Elsevier, 2011.

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4

Robbins, Trevor. The Neuropsycho–Pharmacology of Attention. Editado por Anna C. (Kia) Nobre y Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.028.

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Pharmacological influences on cognition and behaviour are often accompanied by effects on different aspects of attention. The actions of many psychoactive drugs (often used in the treatment of psychiatric disorders) depend on effects exerted on the classical chemical modulatory neurotransmitter systems including acetylcholine, and the monoamines, dopamine, noradrenaline and serotonin (or 5-hydroxytryptamine, 5-HT). These chemical systems originate in the reticular core of the brain and modulate attention by actions on forebrain structures including the thalamus, striatum, and the neocortex (especially the prefrontal cortex). Current research is attempting to dissect separable functions of these chemical neurotransmitters in mediating attention in relation to states of arousal and stress in comparable test paradigms in experimental animals and humans. New directions in research in this area are also identified, including the functions of the novel neurotransmitter orexin, and the role of GABA and glutamate in gamma oscillations and the network properties of the neocortex.
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5

Endoplasmic Reticulum Stress In Health And Disease. Springer, 2012.

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6

Zhang, Kezhong, ed. Endoplasmic Reticulum Stress Response and Transcriptional Reprogramming. Frontiers SA Media, 2015. http://dx.doi.org/10.3389/978-2-88919-436-0.

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7

Agostinis, Patrizia y Samali Afshin. Endoplasmic Reticulum Stress in Health and Disease. Springer Netherlands, 2014.

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8

Agostinis, Patrizia y Samali Afshin. Endoplasmic Reticulum Stress in Health and Disease. Springer London, Limited, 2012.

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9

Wagner, Cameron. Endoplasmic Reticulum Stress: Regulation, Function and Role in Health and Disease. Nova Science Publishers, Incorporated, 2016.

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10

Schäfer, Patrick, Lorenzo Frigerio, Federica Brandizzi y Stephen H. Howell, eds. Endoplasmic reticulum - shape and function in stress translation. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-344-8.

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11

So, Jonathan. Characterization of the endoplasmic reticulum stress response in bipolar-I disorder. 2006.

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12

Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms. Elsevier, 2020. http://dx.doi.org/10.1016/c2019-0-04102-7.

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13

Madkour, Loutfy H. Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms. Elsevier Science & Technology Books, 2020.

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14

Madkour, Loutfy H. Reactive Oxygen Species , Nanoparticles, and Endoplasmic Reticulum Stress-Induced Cell Death Mechanisms: Antioxidant Therapeutic Defenses. Elsevier Science & Technology, 2020.

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15

Siebert, Stefan, Sengupta Raj y Alexander Tsoukas. The genetics of axial spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198755296.003.0004.

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Family and twin studies have long suggested a large genetic component in ankylosing spondylitis (AS). The genetic association with HLA-B27 remains one of the strongest single gene variant associations reported in any complex polygenic disease. The exact mechanism by which HLA-B27 contributes to AS remains unknown, with three main theories proposed: the arthritogenic peptide, endoplasmic reticulum stress with unfolded protein response, and homodimerization theories. Genome-wide association studies have identified a number of other important susceptibility genes for AS, several of which overlap with other spondyloarthritis conditions. Of these, ERAP1 and IL-23R, are covered in more detail, highlighting their functional importance.
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16

Z.Y. Luo, Q. Song, X.P. Xiong, M. Abdulai, H.H. Liu, L. Li, H.Y. Xu, S.Q. Hu y C.C. Han*. The PI3K/Akt/mTOR signaling pathway regulates lipid metabolism mediated by endoplasmic reticulum stress in goose primary hepatocytes. Verlag Eugen Ulmer, 2021. http://dx.doi.org/10.1399/eps.2021.325.

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17

Colbert, Robert A. y Paul Bowness. Immune mechanisms: HLA-B27. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0006.

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HLA-B27 is present in the majority of patients with ankylosing spondylitis (AS). Although we have learned a considerable amount about the natural immunologic function of HLA class I proteins, this has not provided a definitive mechanism of AS pathogenesis. While HLA-B27 is adept at presenting antigenic peptides to CD8+ T cells, ‘arthritogenic’ peptides targeted by a cross-reactive T or natural killer cell response have not been described, nor have autoreactive T cells been found. Newer concepts have evolved based on the propensity of HLA-B27 to ‘misbehave’, both inside cells and on the cell surface. Misfolded HLA-B27 molecules may stimulate an endoplasmic reticulum stress response, promoting production of IL-23 and then IL-17 and related cytokines. Aberrant cell-surface HLA-B27 molecules are ligands for natural killer and related immunoreceptors, and recognition can lead to IL-17 proinflammatory responses. There is growing evidence to suggest that these aberrant behaviours contribute to AS pathogenesis.
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18

Raju, Raghavan y Irshad H. Chaudry. The host response to hypoxia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0305.

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The hypoxic response of the host is complex. While the oxygen-sensing intracellular machinery attempts to restore cellular homeostasis by augmenting respiration and blood flow, events such as severe haemorrhage lead to whole body hypoxia and decreased mitochondrial function. Immunological perturbations following severe haemorrhage may result in multiple organ dysfunction and sepsis, while impaired perfusion may lead to microvascular injury and local hypoxia. Trauma-haemorrhage or hypoxic exposure in animals causes a systemic inflammatory response, decreased antigen presentation by peritoneal macrophages, hypoxaemia and initiation of endoplasmic reticulum stress. In response, the protein level of the oxygen-sensing transcription factor, hypoxia inducible factor (HIF)-1 increases; this leads to the regulation of expression of a number of genes resulting in decreased mitochondrial ATP production, but enhanced glycolytic processes, thus shifting the energy balance. In addition, sustained tissue hypoxia leads to increased free radical production and cellular apoptosis. Though the initial host response to hypoxia may be protective, sustained hypoxia becomes detrimental to the tissues and the organism as a whole.
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19

Hughes, Jeremy. Proteinuria as a direct cause of progression. Editado por David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.

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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease rather than simply acting as a marker of the severity of glomerular injury and podocytes loss. Seminal studies used the atypical renal anatomy of the axolotl to instill proteins directly into the tubular lumen without requiring passage through the glomerulus. This indicated that tubular protein could be cytotoxic and induce interstitial inflammation and fibrosis in the peritubular region. Cell culture studies demonstrate that exposure to proteins results in proximal tubular cell activation and the production of pro-inflammatory and pro-fibrotic mediators. Proximal tubular cell death occurred in some studies reinforcing the potential of protein to exert cytotoxic effects via oxidative stress or endoplasmic reticulum stress. Analysis of renal biopsy material from both experimental studies using models of proteinuric disease or patients with various proteinuric diseases provided evidence of activation of transcription factors and production of chemokines and pro-inflammatory mediators by proximal tubular cells. These data strongly suggest that although proteinuria is the result of glomerular disease it also represents an important cause of progression in patients with chronic kidney disease associated with proteinuria.
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20

Nakamura, Tomohiro y Stuart A. Lipton. Neurodegenerative Diseases as Protein Misfolding Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0002.

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Neurodegenerative diseases (NDDs) often represent disorders of protein folding. Rather than large aggregates, recent evidence suggests that soluble oligomers of misfolded proteins are the most neurotoxic species. Emerging evidence points to small, soluble oligomers of misfolded proteins as the cause of synaptic dysfunction and loss, the major pathological correlate to disease progression in many NDDs including Alzheimer’s disease. The protein quality control machinery of the cell, which includes molecular chaperones as found in the endoplasmic reticulum (ER), the ubiquitin-proteasome system (UPS), and various forms of autophagy, can counterbalance the accumulation of misfolded proteins to some extent. Their ability to eliminate the neurotoxic effects of misfolded proteins, however, declines with age. A plausible explanation for the age-dependent deterioration of the quality control machinery involves compromise of these systems by excessive generation of reactive oxygen species (ROS), such as superoxide anion (O2-), and reactive nitrogen species (RNS), such as nitric oxide (NO). The resulting redox stress contributes to the accumulation of misfolded proteins. Here, we focus on aberrantly increased generation of NO-related species since this process appears to accelerate the manifestation of key neuropathological features, including protein misfolding. We review the chemical mechanisms of posttranslational modification by RNS such as protein S-nitrosylation of critical cysteine thiol groups and nitration of tyrosine residues, showing how they contribute to the pathogenesis of NDDs.
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