Книги: "Intracellular pathways"

1

Perkins, Jonathan Edwards. A study of EGF-induced intracellular signalling pathways and effects in first trimester trophoblast. Birmingham: University of Birmingham, 2003.

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2

Conroy, Louise Anne. The development of t-lymphocytes within the murine foetal thymus: The role of intracellular signalling pathways. Birmingham: University of Birmingham, 1992.

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3

Store-operated Ca2+ entry (SOCE) pathways: Emerging signaling concepts in human (patho)physiology. Wien: Springer, 2012.

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4

Wilks, Andrew F., and Ailsa G. Harpur. Intracellular Signal Transduction: The JAK-STAT Pathway. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4.

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5

Wilks, Andrew F. Intracellular signal transduction: The JAK-STAT pathway. New York: Springer, 1996.

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6

Idestrup, Chris. P2Y-and P2U-purinoceptor activation cause intracellualr CA2+ release in dorsal spinal astrocytes via the phospholipase C[BETA]/IP3 pathway. Ottawa: National Library of Canada, 1996.

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7

Newell-Price, John, Alia Munir, and Miguel Debono. Normal function of the endocrine system. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0182.

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Endocrinology is the study of hormones (and their glands of origin), their receptors, the intracellular signalling pathways they invoke, and their associated diseases. The clinical specialty of endocrinology focuses specifically on the endocrine organs, that is, the organs whose primary function is hormone secretion, including the hypothalamus, the pituitary, the thyroid, the parathyroid, the adrenal glands, the pancreas, and the reproductive organs.

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8

Powell, Craig M. PTEN and Autism With Macrocepaly. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0010.

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Phosphatase and Tensin homolog deleted on chromosome 10 (PTEN) is a gene encoding an intracellular signaling molecule. PTEN was originally discovered as the gene responsible for a subset of familial hamartoma (tumor) syndromes associated with increased risk for certain cancers (Nelen et al., 1997) and as a gene often mutated in human cancers and tumor cell lines (Li et al., 1997; Steck et al., 1997). More recently, mutations in PTEN have been linked genetically to the clinical phenotype of autism or developmental delay with macrocephaly (Boccone et al., 2006; Butler et al., 2005; Buxbaum et al., 2007; Goffin, Hoefsloot, Bosgoed, Swillen, & Fryns, 2001; Herman, Butter, et al., 2007; McBride et al., 2010; Orrico et al., 2009; Stein, Elias, Saenz, Pickler, & Reynolds, 2010; Varga, Pastore, Prior, Herman, & McBride, 2009; Zori, Marsh, Graham, Marliss, & Eng, 1998). This chapter examines the role of PTEN in intracellular signaling, the link between PTEN signaling pathways and other autism-related genes and signaling pathways, the genetic relationship between PTEN and autism, model systems in which effects of Pten deletion on the brain have been studied, and promising preclinical data identifying therapeutic targets for patients with autism/macrocephaly associated with PTEN mutations.

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9

Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.

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10

Harpur, Ailsa G., and Andrew F. Wilks. Intracellular Signal Transduction: The JAK-STAT Pathway. Springer, 2013.

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11

Wilks, Andrew F. Intracellular Signal Transduction: The Jak-Stat Pathway. Springer, 2013.

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12

Monaco, Claudia, and Giuseppina Caligiuri. Molecular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0014.

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The development of the atherosclerotic plaque relies on specific cognate interactions between ligands and receptors with the ability to regulate cell recruitment, inflammatory signalling, and the production of powerful inflammatory and bioactive lipid mediators. This chapter describes how signalling is engaged by cell-cell surface interactions when the endothelium interacts with platelets and leukocytes enhancing leukocyte recruitment during atherogenesis. It also exemplifies intracellular signalling pathways induced by the activation of innate immune receptors, the most potent activators of inflammation in physiology and disease. Differences are highlighted in innate signalling pathways in metabolic diseases such as atherosclerosis compared to canonical immunological responses. Finally, the key lipid mediators whose production can affect endothelial function, inflammation, and atherosclerosis development are summarized. This Chapter will take you through these fundamental steps in the development of the atherosclerotic plaque by summarizing very recent knowledge in the field and highlighting recent or ongoing clinical trials that may enrich our ability to target cardiovascular disease in the future.

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13

Oren, Moshe, and Yael Aylon. Hippo Signaling Pathway and Cancer. Springer London, Limited, 2013.

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14

The Hippo Signaling Pathway And Cancer. Springer-Verlag New York Inc., 2013.

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15

Oren, Moshe, and Yael Aylon. The Hippo Signaling Pathway and Cancer. Springer, 2015.

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16

Rosengart, Matthew R. Disorders of calcium in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0253.

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Calcium is vitally important for normal cellular signalling and function. However, its toxicity necessitates that intracellular calcium concentration [Ca2+] be tightly regulated and compartmentalized. Evolutionary pressures have yielded several regulatory mechanisms to maintain intracellular and extracellular ionized calcium concentrations compatible with life. During periods of critical illness these process are commonly overwhelmed, and disorders of calcium homeostasis are highly prevalent among intensive care unit (ICU) patients. Indeed, hypocalcaemia occurs in up to 88% of critically-ill ICU patients suffering from trauma, sepsis, and burns. Contemporary evidence suggests that although hypocalcaemia may be associated with ICU mortality, it is not in the causal pathway. A systematic review concluded there are no data to support the routine parenteral administration of calcium in the management of asymptomatic critical illness-related hypocalcaemia. Asymptomatic hypocalcaemia of critical illness does not necessitate replacement. However, acute, symptomatic hypocalcaemia necessitates parenteral supplementation to prevent tetany, seizures, and cardiac arrhythmias

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17

Briddon, Anthony. Approach to the Patient with Hyperhomocysteinemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0079.

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Hyperhomocysteinaemia (HHC) may occur as a result of a variety of inherited and acquired conditions ranging from mild and benign to severe and life threatening, and there is a higher probability that they will first manifest during early adulthood rather than infancy, with acquired forms commonly presenting into old age. Milder forms of HHC may exist without homocystinuria, and screening tests relying on the presence of homocystine in the urine will give a false negative result. Methylcobalamin is an essential cofactor for methionine synthase, a key enzyme in the homocysteine remethylation pathway: consequently, investigation for inherited abnormalities of intracellular B12 metabolism forms an integral part of the biochemical investigation of HHC. Additionally, there are acquired forms of HHC, notably those involving vitamin B12 deficiency and malabsorption. Mild to moderate HHC has also been associated with alcohol abuse, excessive caffeine intake, hypothyroidism, and poor renal function.

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18

Skipworth, James R. A., and Stephen P. Pereira. Pathophysiology, diagnosis, and assessment of acute pancreatitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0190.

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The incidence of acute pancreatitis continues to increase, but the attendant mortality has not decreased for >30 years. The pathogenesis remains poorly understood, but the initial mechanism appears to be intracellular activation of pancreatic enzymes, with micro- and macrovascular dysfunction, in conjunction with a systemic inflammatory response acting as a key propagating factor and determinant of severity. A multitude of causes or initiators exist, but there is a common pathophysiological pathway. The use of conventional scoring systems, combined with repeated clinical and laboratory assessment, remain the optimal method of predicting early severity and organ dysfunction. Death occurs in a biphasic pattern with early mortality (<2 weeks) secondary to SIRS and MODS; and late deaths (>2 weeks) due to superinfection of pancreatic necrosis. Assessment of severity should reflect this, with early severity being diagnosed in the presence of organ failure for >48 hours, and late severity defined by the presence of pancreatic and peri-pancreatic complications on CT or other appropriate imaging modalities.

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19

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0032.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.

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20

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_001.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.

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21

Casaer, Michael P., and Greet Van den Berghe. Nutrition support in acute cardiac care. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0032_update_002.

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Malnutrition in cardiac and critical illness is associated with a compromised clinical outcome. The aim of nutrition therapy is to prevent these complications and particularly to attenuate lean tissue wasting and the loss of muscle force and of physical function. During the last decade, several well-powered randomized controlled nutrition trials have been performed. Their results challenge the existing nutrition practices in critically ill patients. Enhancing the nutritional intake and the administration of specialized formulations failed to evoke clinical benefit. Some interventions even provoked an increased mortality or a delayed recovery. These unexpected new findings might be, in part, caused by an important leap forward in the methodological quality in the recent trials. Perhaps reversing early catabolism in the critically ill patient by nutrition or anabolic interventions is impossible or even inappropriate. Nutrients effectively suppress the catabolic intracellular autophagy pathway. But autophagy is crucial for cellular integrity and function during metabolic stress, and consequently its inhibition early in critical illness might be deleterious. Evidence from large nutrition trials, particularly in acute cardiac illness, is scarce. Nutrition therapy is therefore focused on avoiding iatrogenic harm. Some enteral nutrition is administered if possible and eventually temporary hypocaloric feeding is tolerated. Above all, the refeeding syndrome and other nutrition-related complications should be prevented. There is no indication for early parenteral nutrition, increased protein doses, specific amino acids, or modified lipids in critical illness.

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