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1
Altenmüller, Eckart. Music, the brain, and music learning: Mental representation and changing cortical activation patterns through learning. Narberth, PA: Gordon Institute for Music Learning, 1997.
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2
Shafi, Mouhsin M., and M. Brandon Westover. EEG Activation Methods. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0010.
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Activation procedures are commonly employed to increase the diagnostic yield of electroencephalography (EEG) in patients with suspected epilepsy. This chapter reviews the effects and utility of hyperventilation, intermittent photic stimulation, and color/pattern stimulation on the EEG in patients with epilepsy and other neurological disorders. In theory, the greater the number of different activation methods used in EEG evaluation of an epilepsy patient, the greater the chance of obtaining abnormal findings. However, the specificity of these findings for epilepsy is uncertain. Furthermore, from a practical point of view, desirable activations are those methods that can be carried out easily and systematically, in a short time frame, with affordable equipment, without undesirable side effects for patients, and with reliable and predictive results. At this time, hyperventilation and intermittent photic stimulation are the most widely used activation methods and have an extensive body of literature supporting them.
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Segall, Liviu, and Adrian Covic. Immune-mediated tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0093_update_001.
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Immune-mediated tubulointerstitial nephritides (TINs) are generally encountered in the context of systemic or extrarenal autoimmune diseases, such as sarcoidosis, Sjögren syndrome, systemic lupus erythematosus, inflammatory bowel disease, TIN and uveitis (TINU) syndrome, and immunoglobulin G4-related disease. The pathogenesis of these TINs is complex and more or less unclear; it usually involves leucocyte activation, autoantibodies, immune complex deposition, complement activation, and release of inflammatory cytokines and growth factors. Tubulointerstitial inflammation most commonly has a chronic pattern, although acute forms of TIN may also occur. Furthermore, inflammation may be granulomatous (as in sarcoidosis or Crohn’s disease) or non-granulomatous. Immunofluorescence staining can sometimes reveal immune complex deposits and even antitubular basement membrane autoantibodies. Systemic immunosuppressive therapies are almost always required to prevent progression to irreversible interstitial fibrosis, tubular atrophy, and end-stage renal disease.
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Wiersinga, W. Joost, and Tom van der Poll. The host response to infection in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0303.
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Infection continues to be a leading cause of intensive care unit death. The host response to infection can be seen as a pattern recognition receptor (PRR)-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. A measured and rapid response to microbial invasion is essential to health. The same immunological and coagulation systems that protect against localized infection can act to our disadvantage when these systems are activated systemically during generalized microbial infection. Toll-like receptors (TLR), the inflammasomes and other PRRs initiate the host response after recognition of pathogen-associated-molecular-patterns (PAMPs) or endogenous danger-associated-molecular-patterns (DAMPs). The systemic host response to infection will result in activation of coagulation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Further dissection of the role of host–pathogen interactions, the cytokine response, the coagulation cascade and their multidirectional interactions in sepsis should lead towards the development of new therapeutic approaches in the critically ill who are faced with infection.
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Geri, Guillaume, and Jean-Paul Mira. Host–pathogen interactions in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0306.
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Infection by a pathogenic micro-organism triggers a coordinated activation of both innate and adaptive immune responses. The innate immune response quickly triggers an antimicrobial response that will initiate development of a pathogen-specific, long-lasting adaptive immune response. Accurate recognition of microbial-associated molecular patterns by pattern-recognition receptors (PRRs) is the cornerstone of this immediate response. Most studied PRRs are Toll-like receptors (TLRs) and their kinase signalling cascades that activate nuclear transcription factors, and induce gene expression and cytokine production. Deficiencies or genetic variability in these different signalling pathways may lead to recurrent pyogenic infections and severe invasive diseases. After initial contact between the host and pathogen, numerous factors mediate the inflammatory response, as pro-inflammatory cytokines and chemokines. Apart from host genetic variability, pathogen diversity also influences the phenotypic features of various infectious diseases. Genomic analysis may assist in the development of targeted therapies or new therapeutic strategies based on both patient and microorganism genotype.
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Sampson, Heidi. Characterization of Drosophila nuclear receptor interactions and activation patterns. 2006.
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7
Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.
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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
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Covassin, Naima, and Virend K. Somers. The cardiovascular system during sleep. Edited by Guido Grassi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0028.
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The majority of molecular, physiological, and behavioural processes undergo substantial variations across a 24 h period. The health implications of such fluctuations, whether they are expressions of an intrinsic circadian rhythmicity or are secondary to changes in physical activity, posture, and/or sleep, are increasingly recognized. Similar to other biological functions, the cardiovascular system exhibits a prominent day–night profile, with profound haemodynamic, autonomic, and hormonal oscillations occurring during the sleep period. These time-dependent and sleep stage-dependent patterns of function have important clinical significance. The cardiovascular downregulation achieved throughout the night while asleep may be restorative and protective against adverse events, while the morning physiological activation coincident with awakening facilitates resumption of daytime activities. Nevertheless, rather than beneficial, these activity configurations may be pathogenic in individuals with a vulnerable substrate and may favour onset and progression of cardiovascular diseases. Cardiovascular complications may also arise as a consequence of abnormal day–night periodicity and disturbed sleep quantity and quality. Hence, consideration of the diurnal pattern of cardiovascular activity is critical in the clinical setting.
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Bind, Rebecca Hannah, and Carmine M. Pariante. Psychoneuroimmunology of Post-Traumatic Stress Disorder. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0021.
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This chapter reviews the evidence linking post-traumatic stress disorder (PTSD) with changes in immune function. The chapter starts with a brief explanation of the components of the immune system, including cytokines, and of the mechanisms linking psychological and psychiatric phenomena with changes in immune function (i.e., psychoneuroimmunology). Specific studies on PTSD are then described, including the potential neurobiological and health consequences of these immune changes and, finally, the effects of PTSD treatment on both symptomology and the immune system. While there is a consistent pattern of findings indicating increased immune activation in this condition, there is a paucity of research on the immunological correlates of PTSD, especially compared with the large number of immunological studies on depression and other psychiatric disorders.
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Borsboom, Denny. Mental disorders, network models, and dynamical systems. Edited by Kenneth S. Kendler and Josef Parnas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198796022.003.0011.
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Network approaches have been proposed as an alternative way of thinking about relations between symptoms of mental disorders. Unlike traditional psychometric approaches, network models view these associations as the result of direct interactions between symptoms. Disorders are defined as alternative stable states of a network due to increased connectivity between symptoms. This increased connectivity creates a pattern of reinforcement, so the system can get stuck in a state of prolonged activation. Mental health is defined as the stable state of a weakly connected network. Although symptomatology may be temporarily increased in a healthy network (e.g., due to adverse life events), as the influence of a shock wanes the network will spontaneously return to its healthy state. Strongly connected networks, however, may transition into disordered states upon similar external shocks, and may not naturally recover. Thus, the proposed definitions yield plausible conceptualizations of resilience and vulnerability.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.
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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
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Schwartz, Peter J., and Lia Crotti. Monogenic and oligogenic cardiovascular diseases: genetics of arrhythmias—catecholaminergic polymorphic ventricular tachycardia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0152.
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Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare inherited disorder associated with syncope and sudden death manifesting in the young during sympathetic activation. The electrocardiogram is normal and the heart is structurally normal. The diagnosis is usually made with an exercise stress test that shows a typical pattern of onset and offset of adrenergically induced ventricular arrhythmias. Molecular screening of RyR2, the major CPVT gene, is recommended whenever the suspicion of CPVT is high. If a disease-causing mutation is identified, cascade screening allows pre-symptomatic diagnosis among family members. All affected subjects should be treated with beta blockers (nadolol or propranolol). Preliminary data support the association of beta blockers with flecainide. After a cardiac arrest, an implantable cardioverter defibrillator (ICD) should be implanted, but it is accompanied by a disquietingly high incidence of adverse effects. After syncope on beta blocker therapy, left cardiac sympathetic denervation is most effective, preserves quality of life, and does not preclude a subsequent ICD implantation.
13
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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Rubia, Katya. ADHD brain function. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198739258.003.0007.
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ADHD patients appear to have complex multisystem impairments in several cognitive-domain dissociated inferior, dorsolateral, and medial fronto-striato-parietal and frontocerebellar neural networks during inhibition, attention, working memory, and timing functions. There is emerging evidence for abnormalities in motivation and affect control regions, most prominently in ventral striatum, but also orbital/ventromedial frontolimbic areas. Furthermore, there is an immature interrelationship between hypoengaged task-positive cognitive control networks and a poorly ‘switched off’ default mode network, both of which impact performance. Stimulant medication enhances the activation of inferior frontostriatal systems, while atomoxetine appears to have more pronounced effects on the dorsal attention network. More studies are needed to understand the neurofunctional correlates of the effects of age, gender, ADHD subtypes, and comorbidities with other psychiatric conditions. The use of pattern recognition analyses applied to imaging to make individual diagnostic or prognostic predictions are promising and will be the challenge over the next decade.
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Ali, Ased. Pathogenesis of urinary tract infection. Edited by Rob Pickard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0001.
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The realization of the harms resulting from indiscriminate use of antibiotics for minor infection has added impetus to the need to understand better the interaction between urogenital tract epithelium and invading bacteria during the initial stages of urinary tract infection (UTI). It is thought that uropathogenic Escherichia coli clones develop in the gut and migrate across the perineum to the urethra and up into the bladder. The response of the epithelium to bacterial adherence and the evolution of the invading bacteria will then govern the clinical consequences. These can vary between rapid invasion and further migration to produce systemic sepsis to tolerance of the bacteria in a planktonic state in asymptomatic bacteriuria. The key to these differences is the activation of epithelial pathogen-associated molecular pattern receptors by expressed proteins on the bacterial cell wall. Increased understanding of these interactions will lead to non-antibiotic-based strategies for clinical management of urinary infection.
16
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
17
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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Buckley, Bernadette Drew. Comparison of muscle activation pattens in boys and girls during a simple landing task. 2003.
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19
Baildam, Eileen. Juvenile idiopathic arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0116.
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Juvenile idiopathic arthritis (JIA) is defined as arthritis lasting for 6 weeks or more presenting in childhood at any age up to 17 years. Arthritis is diagnosed clinically by the presence of joint pain, stiffness, and swelling with inflammation limiting the range of individual joint movement. There are subtypes that tend to follow distinct courses and with phenotypes that vary widely from a serious systemic inflammatory disorder of systemic JIA to single-joint monoarthritis. The differential diagnosis of JIA is wide and the best chance of long-term remission is where treatment is started as early as possible. However, there is often delay in diagnosis in childhood and there is no single reliable diagnostic test so pattern recognition is fundamental. There are associated disorders such as silent uveitis that must be screened for and managed as part of essential multidisciplinary care. Systemic JIA is complicated by potentially life-threatening macrophage activation syndrome that is often underdiagnosed but where the diagnosis is based on easy clinical tests and where awareness is vital. This chapter covers descriptions of the classification criteria for chronic arthritis in children, clinical presentations and likely course for the various subtypes.
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Zamarian, L., and Margarete Delazer. Arithmetic Learning in Adults. Edited by Roi Cohen Kadosh and Ann Dowker. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199642342.013.007.
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Neuroimaging has significantly contributed to our understanding of human learning by tracking the neural correlates underlying the acquisition of new expertise. Studies using functional magnetic resonance imaging (fMRI) suggest that the acquisition of arithmetic competence is reflected in a decrease of activation in frontal brain regions and a relative increase of activation in parietal brain regions that are important for arithmetic processing. Activation of the angular gyrus (AG) is related to fact learning, skilled retrieval, and level of automatization. fMRI investigations extend the findings of cognitive studies showing that behavioural differences between trained and untrained sets of items, between different arithmetic operations, and between different training strategies are reflected by specific activation patterns. fMRI studies also reveal inter-individual differences related to arithmetic competence, with low performing individuals showing lower AG activation when answering calculation problems. Importantly, training attenuates inter-individual differences in AG activation. Studies with calculation experts suggest that different strategies may be used to achieve extraordinary performance. While some experts recruit a more extended cerebral network compared with the average population, others use the same frontoparietal network, but more efficiently. In conclusion, brain imaging studies on arithmetic learning and expertise offer a promising view on the adaptivity of the human brain. Although evidence on functional or structural modifications following intervention in dyscalculic patients is still scarce, future studies may contribute to the development of more efficient and targeted rehabilitation programmes after brain damage or in cases of atypical numerical development.
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Stamatakis, Emmanuel A., Eleni Orfanidou, and Andrew C. Papanicolaou. Functional Magnetic Resonance Imaging. Edited by Andrew C. Papanicolaou. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199764228.013.7.
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Functional magnetic resonance imaging (fMRI) is the most frequently used functional neuroimaging method and the one that accounts for most of the neuroimaging literature. It measures the blood oxygen level-dependent (BOLD) signal in different parts of the brain during rest and during task-induced activation of functional networks mediating basic and higher functions. A basic understanding of the various instruments and techniques of recording the hemodynamic responses of different brain regions and the manner in which we establish activation and connectivity patterns out of these responses is necessary for an appreciation of the contemporary functional neuroimaging literature. To facilitate such an understanding is the purpose of this chapter.
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Dutto, Darren John. Leg spring model related to muscle activation, force, and kinematic patterns during endurance running to voluntary exhaustion. 1999.
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23
Becker, Jeffrey. Nutraceutical Treatments for Addiction Recovery. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0020.
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Current medical treatment in substance-use disorders and addiction recovery often fails to address the underlying molecular pathophysiologic mechanisms of addiction morbidity. Psychopharmacology and behavioral interventions do not directly address the cellular patterns of dysfunction in addiction but natural treatments can and should be employed in a research-based manner to support existing treatment protocols. Research into addiction pathophysiology is clear: removing the offending agent through sobriety is often not enough to restore natural premorbid physiology. Drug-induced oxidative stress and inflammation may inhibit full recovery by damaging molecular health, homeostasis, and neurological function. Prolonged activation of stress systems likely affects judgment during the “white-knuckle” stage of recovery. The author discusses research characterizing the following 3 functional categories of addiction pathophysiology: inflammation and antioxidant system degradation, stress system activation, and vitamin and mineral depletion patterns. Each section is followed by discussion of research-based natural treatments employed to support addiction recovery at the cellular level.
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Stanworth, Simon, and Stuart McKechnie. Pathophysiology of disordered coagulation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0269.
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Imbalances in the regulation of haemostasis may manifest as bleeding (depletion of pro-coagulant factors) or thrombosis (deficiency of anti-coagulants). Disordered haemostasis is common in critically-ill patients and may result from infection, trauma, haemorrhage, inflammation, organ dysfunction (notably renal and liver dysfunction), or drug therapy. Complex patterns of coagulopathy where both bleeding and prothrombotic tendencies co-exist are well recognized in critical illness. The limitations of standard laboratory coagulation tests to predict bleeding risk, including activated partial thromboplastin time and prothrombin time, are well recognized. These assays were developed for diagnosis of inherited bleeding disorders or for monitoring of anticoagulant therapy. This has led to increased interest in global haemostatic tests, such as viscoelastic and thrombin generation tests. Thromboembolism is an important cause of morbidity and mortality in critically-ill patients. While inherited causes of bleeding appear to be often related to single gene abnormalities, thrombotic tendencies appear to reflect more complex interactions between inherited and acquired factors. Many interactions exist between coagulation pathways and inflammation. Systemic inflammation triggers widespread activation of coagulation, with pro-inflammatory cytokines activating pro-coagulant pathways and downregulating anticoagulant pathways. A net result of this interaction between inflammatory and coagulation pathways in sepsis is thrombin generation, intravascular fibrin deposition and a consumptive coagulopathy.
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Brail, Leslie Harris. Analysis of the expression patterns of plasminogen activator genes at the single cell level. 1999.
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26
Bisschops, Raf. Ligand & Electrically Induced Activation Patterns in Myenteric Neuronal Networks: Confocal Calcium Imaging As a Bridge Between Basic & Human Physiology (Acta Biomedica Lovaniensia). Leuven Univ Pr, 2005.
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27
PALACE, Kriss. Activating the Power of Your Creative Mind: Super Ideas to Build Creative Patterns for Achieving Success and Harmony. Independently Published, 2022.
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Alavi, Abass, and Andrew B. Newberg. Functional Neuroimaging: A Transformative Tool for Integrative Psychiatry. Edited by Anthony J. Bazzan and Daniel A. Monti. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190690557.003.0014.
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Functional neuroimaging with positron emission tomography (PET), single photon emission computed tomography (SPECT), and functional magnetic resonance imaging (fMRI) can be highly useful in the evaluation and management of patients with psychiatric disorders. PET and SPECT imaging typically evaluate cerebral metabolism and blood flow, respectively, and can determine patterns associated with different disorders such as depression or schizophrenia. PET and SPECT imaging can also evaluate neurotransmitter changes such as dopamine or serotonin associated with different psychiatric disorders. fMRI is an excellent tool for studying the effects of psychiatric disorders on specific brain processes related to cognition and mood. fMRI activations studies allow researchers to present various stimuli to a subject in order to determine how the brain reacts and whether psychiatric disorders are associated with different brain reactivity patterns. Functional neuroimaging with PET, SPECT, and fMRI can be highly useful in the investigation of the mechanism of action of integrative therapies for psychiatric disorders.
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Gordon, Edwin E., Eckart Altenmuller, and Wilfried Gruhn. Music, the Brain, and Music Learning: Mental Representation and Changing Cortical Activation Patterns Through Learning : Taking Another Look at the Established Procedure for Scoring the ad. G I a Pubns, 2000.
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Hoftman, Gil D., and Dean F. Salisbury. Neurobiology of Schizophrenia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199331505.003.0005.
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Schizophrenia is a brain disease with unknown etiology; a variety of neurodevelopmental mechanisms contribute to its pathogenesis. In this chapter, we review some of the most salient neurobiological findings that seem to be linked with the pathophysiology of psychosis generally and schizophrenia specifically. Several important findings have been made from neuroimaging and neuropathology, including reduced whole-brain volume, enlarged ventricles, and decreased cortical gray matter. Abnormalities in the prefrontal cortex, such as decreased dendritic spine density, are particularly important for cognitive and negative symptoms in schizophrenia. Functional imaging suggests that patterns of activation may be closely linked to symptom clusters. We will review neurotransmitter abnormalities, especially dopamine but also glutamate and GABA, and relevant circuitry and connectivity problems related to pathology. Finally, we will discuss genetics and heritability, and the challenges of identifying relevant loci in such a complex disorder.
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Bearman, Peter, and Peter Hedström, eds. The Oxford Handbook of Analytical Sociology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oxfordhb/9780199215362.001.0001.
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This book explores analytical sociology as an approach for explaining important social facts such as network structures, patterns of residential segregation, typical beliefs, and cultural tastes. It brings together some of the most prominent analytical sociologists in Europe and the United States in an effort to clarify the distinctive features of the approach and to further its development. The volume is organized into four parts. Part I describes the foundations of analytical sociology while Part II discusses the role of action and interaction in explaining diverse social processes such as emotions and beliefs. Part III looks at the macroscopic social dynamics brought on by the activation of the cog-and-wheel mechanisms, tackling topics ranging from segregation dynamics to divorce and social influence. Part IV concludes the book by asking how analytic sociology relates to other fields and approaches such as game theory, analytic ethnography, and historical sociology.
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Vaghi, M. M., and T. W. Robbins. Task-Based Functional Neuroimaging Studies of Obsessive-Compulsive Disorder: A Hypothesis-Driven Review. Edited by Christopher Pittenger. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228163.003.0022.
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The neurobiological basis of Obsessive Compulsive Disorder (OCD) has been probed using functional magnetic resonance in hundreds of studies over three decades. This complex literature can be syntheized using a theory-informed approach. At a theoretical level, separable, independent, constructs of relevance to OCD have been identified. At the experimental level, extensive translational evidence has provided an account that relates specific brain systems to these neuropsychological constructs. Parallels between neural substrates implicated in OCD and functional specialization of different brain regions suggest that abnormalities within fronto-striatal circuitry impinge on executive functions, and their subcomponents, and on goal-directed learning and habit formation. In OCD, this is reflected at a functional level in patterns of abnormal activations in particular brain regions during specific cognitive tasks. However, many issues still need to be addressed. The authors suggest that the experimental context might represent a pivotal variable that should be taken into account.
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Prasad, Girijesh. Brain–machine interfaces. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199674923.003.0049.
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A brain–machine interface (BMI) is a biohybrid system intended as an alternative communication channel for people suffering from severe motor impairments. A BMI can involve either invasively implanted electrodes or non-invasive imaging systems. The focus in this chapter is on non-invasive approaches; EEG-based BMI is the most widely investigated. Event-related de-synchronization/ synchronization (ERD/ERS) of sensorimotor rhythms (SMRs), P300, and steady-state visual evoked potential (SSVEP) are the three main cortical activation patterns used for designing an EEG-based BMI. A BMI involves multiple stages: brain data acquisition, pre-processing, feature extraction, and feature classification, along with a device to communicate or control with or without neurofeedback. Despite extensive research worldwide, there are still several challenges to be overcome in making BMI practical for daily use. One such is to account for non-stationary brainwaves dynamics. Also, some people may initially find it difficult to establish a reliable BMI with sufficient accuracy. BMI research, however, is progressing in two broad areas: replacing neuromuscular pathways and neurorehabilitation.
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Ólafsson, Stefán, Mary Daly, Olli Kangas, and Joakim Palme, eds. Welfare and the Great Recession. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198830962.001.0001.
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This book surveys and analyses the welfare consequences of the Great Recession in Europe and investigates how the burdens of the crisis were shared—between countries, between different socio-economic groups across Europe, and within individual countries. The studies are based on broad comparisons of 30 countries and deeper analyses of 9 country cases. The approach is grounded in classical theories about crisis responses and relates financial hardship to institutional characteristics—such as welfare regimes, currency regimes, socio-political patterns, affluence levels, public debt, and policy reactions during the crisis period—for example, stimulus versus austerity, the degree of social protection emphasis, the commitment to redistribution, and the significance of activation. Welfare and the Great Recession offers new evidence on and demonstrates the importance of the welfare state and government policies with regard to sheltering populations from the level of living consequences of serious economic contraction and distributing burdens in a crisis situation. The book offers various lessons from the crisis experience in Europe and ends with a discussion about welfare futures in a globalized, crisis-prone environment.
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Lewis, Marc D. The Development of Emotion Regulation. Edited by Philip David Zelazo. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199958474.013.0004.
Full textAbstract:
This chapter examines the relation between normative advances and emerging individual differences in emotion regulation (ER), using principles from developmental cognitive neuroscience to integrate these seemingly disparate processes. Like several other theorists, I view corticolimbic development as a self-organizing stream of synaptic alterations, driven by experience rather than biologically prespecified. This conceptualization helps resolve ambiguities that appear when we try, but consistently fail, to neatly parse individual differences and developmental differences. At the neural level, increasingly specific patterns of synaptic activation converge in response to (or in anticipation of) recurrent emotions, creating synaptic networks that link multiple regions. These networks regulate emotions (in real time). But they also stabilize and consolidate with repetition, thus giving rise tohabitsthat are the hallmark of individual development. These configurations are progressively sculpted through individual learning experiences, but they also become increasingly effective with use, thereby expressing both individual trajectories and normative advances as they develop. In sum, experience-driven synaptic changes create a repertoire of individual solutions to universal challenges, shared among members of a culture or society. This description casts individual differences and age-related advances as dual facets of a unitary developmental process.
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Berger, Tobias. Translating Institutions. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198807865.003.0006.
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This chapter proves the decisive importance of local translators. It analyses a large-scale social experiment that is built into the development project aimed at activating the village courts. Whereas in four regions it is implement by a local NGO, in a fifth region it is directly run by the experts of international donor agencies. In this region, the project clearly fails to change established patterns of conflict resolution. In the other four regions, however, the NGO fieldworkers have enhanced access to local authorities for marginalized people by introducing village courts. They do not do so as anticipated by their international donors who want the village courts to become an extension of the state-backed rule of law—but instead of adhering to strict substantial and procedural requirements, the fieldworkers translate the institution of the village courts by integrating them into the universe of non-state justice institutions in rural Bangladesh.
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Denton, Christopher P., and Pia Moinzadeh. Systemic sclerosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0121.
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The term 'scleroderma' describes a group of conditions in which the development of thickened, fibrotic skin is a cardinal feature. This includes localized forms of scleroderma (e.g. morphoea) and also systemic forms of the disease that are more correctly termed systemic sclerosis. Systemic sclerosis (SSc) is a multiorgan, autoimmune disease that has a high clinical burden and mortality, due to affecting the skin as well as internal organs. As with other related diseases there is a female predominance and marked clinical diversity. The pathogenesis of SSc is not fully elucidated; it includes endothelial cell injury fibroblast activation and autoimmunity that lead to skin and internal organ manifestations. The majority of cases exhibit characteristic serum autoantibodies. Some of these antibodies are scleroderma-specific reactivities including anti-centromere (ACA), anti-topoisomerase-1 (ATA or Scl 70) or anti-RNA polymerase III antibodies. These anti-nuclear antibody (ANA) patterns are generally mutually exclusive and serve as useful clinical markers of disease subgroups. Additional subsetting of scleroderma cases, based on the extent of skin sclerosis, permits classification into limited and diffuse subsets. Because of the heterogeneity of the disease patients may suffer from different organ manifestations, such as lung fibrosis, hypertensive renal crisis, severe cardiac disease, gastrointestinal involvement, and pulmonary arterial hypertension. Although outcomes have improved recently, systemic sclerosis still has the highest case-specific mortality of any of the autoimmune rheumatic diseases and requires careful and systematic investigation, management and follow-up. Treatment includes symptomatic strategies with attention to each involved organ system; it is still an area where therapeutic progress and better understanding of pathogenesis is increasingly anticipated.
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Kohn, Livia. The Daode Jing. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780190689810.001.0001.
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The Daode jing (Book of the Dao and Its Virtue) is an essential work in both traditional Chinese culture and world philosophy. The oldest text of philosophical Daoism, and also widely venerated among religious Daoist practitioners, it was around the fourth century BCE, ascribed to a thinker contemporaneous to Confucius (551–479 BCE) named Laozi. Written in aphoristic verse, the book survives in several manuscripts, and its standard version consists of eighty-one chapters and two parts, one on Dao (chs. 1–37), and one on De (chs. 38–81), in approximately five thousand characters. Today, the Daode jing is still actively used in Daoist practice but, more importantly, serves as an inspirational guide to people in China and throughout the world. Its key concepts include cosmological notions, such as Dao, the underlying power of all life and the way the world functions; virtue or inner power, the manifestation of Dao within individual and society; heaven, the representative of nature and the patterns of stars, seasons, and more; as well as yin and yang, the alternating waves of universal development. In addition, it also presents key personal values, such as individual authenticity in so-being (aka naturalness or spontaneity), an ease and flow of life in nonaction, as well as integrity, humility, frugality, softness, simplicity, sufficiency, and more. Guides to Sacred Texts: The Daode jing by Livia Kohn presents a comprehensive overview of information regarding the Daode jing, from its origins and history through its content, commentaries, and ritual activation to its impact in the modern world, including self-help guides, leadership manuals, and poetic, even outlandish renditions.