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Bibliographies thématiques / Onset of diseases / Livres

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Livres sur le sujet « Onset of diseases »

Auteur : Grafiati

Publié le 7 juin 2025

Mis à jour le 2 août 2025

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1

Zoeteweij, M. W., and P. S. Harper. Prenatal Testing for Late-Onset Neurogenetic Diseases. Edited by G. Evers-Kiebooms. Taylor & Francis, 2002. http://dx.doi.org/10.4324/9780203450291.

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G, Evers-Kiebooms, Zoeteweij M. W, and Harper Peter S, eds. Prenatal testing for late-onset neurogenetic diseases. BIOS Scientific, distributed exclusively in the United States and Canada by Springer-Verlag New York, 2002.

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3

1927-, Butler Robert N., and Brody Jacob A. 1931-, eds. Delaying the onset of late-life dysfunction. Springer Pub. Co., 1995.

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4

Smith, David G. Understanding M.E.: The phenomenon of myalgic encephalomyelitis and acute onset post viral fatigue syndrome. Robinson Publishing, 1989.

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5

Smith, David G. Understanding M.E.: The phenomenon of myalgic encephalomyelitis and acute onset post viral fatigue syndrome. Robinson Publishing, 1991.

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6

Melissa, Pearrow, and Jimerson Shane R, eds. Identifying, assessing, and treating early onset schizophrenia at school. Springer, 2010.

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7

Parker, James N., and Philip M. Parker. Infantile-onset ascending hereditary spastic paralysis: A bibliography and dictionary for physicians, patients, and genome researchers [to internet references]. ICON Health Publications, 2007.

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8

Wang, Lemin. The Origin and Onset of Thrombus Disease. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7344-1.

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9

Raymond, Levy, ed. Clinical diversity in late onset Alzheimer's disease. Oxford University Press, 1992.

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10

Durno, Carol Anne. Mode of inheritance and demographics of pediatric-onset inflammatory bowel disease. National Library of Canada, 1999.

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11

Brunner, Hermine Isabella. Investigation of the relationship between disease activity and disease damage in childhood-onset systemic lupus erythematosus. National Library of Canada, 2001.

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12

Rainey, Susan. Molecular characterization of a variant chromosome 22 associated with late onset Alzheimer Disease. National Library of Canada, 1993.

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13

Reiswig, Gary. The thousand mile stare: Unraveling the mystery of early onset Alzheimer's : one family's legacy. Nicholas Brealey Pub., 2009.

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14

Nicole, Baumann, Federico Antonio, and Suzuki Kunihiko, eds. Late onset neurometabolic genetic disorders: From clinical to molecular aspects of lysosomal and peroxisomal disease. Karger, 1991.

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15

Evers-Kiebooms. Prenatal Testing for Late Onset Neurological Diseases. Garland Science, 2002.

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16

Evers-Kiebooms, G., Peter Harper, and M. W. Zoeteweij. Prenatal Testing for Late-Onset Neurogenetic Diseases. Taylor & Francis Group, 2002.

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17

Evers-Kiebooms, G., P. Harper, and M. Zoetweij. Prenatal Testing for Late-Onset Neurogenetic Diseases. Taylor & Francis Group, 2002.

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18

Burgos-Vargas, Ruben, and Shirley M. L. Tse. Juvenile-onset spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0015.

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Juvenile-onset spondyloarthritis (JoSpA) refers to the group of HLA-B27-associated paediatric rheumatic diseases that involves the synovium and entheses of peripheral joints in the initial years and, in some patients, the sacroiliac and spinal joints several years later. Patients with JoSpA may also have extra-articular manifestations, including anterior uveitis, psoriasis and inflammatory bowel disease (IBD), and this represents a disease continuum with adult-onset SpA. JoSpA might include patients with enthesitis-related arthritis (ERA) and PsA categories of juvenile idiopathic arthritis (JI

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19

Costanzi, Marco, ed. Predicting Psychopathological Onset: Early Signs of Neuropsychiatric Diseases. MDPI, 2022. http://dx.doi.org/10.3390/books978-3-0365-4541-7.

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20

Hanas, Ragnar, Andrea Scaramuzza, and Carine de Beaufort. Research into Childhood-Onset Diabetes: From Study Design to Improved Management. Springer, 2016.

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Hanas, Ragnar, Andrea Scaramuzza, and Carine de Beaufort. Research into Childhood-Onset Diabetes: From Study Design to Improved Management. Springer, 2018.

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Hanas, Ragnar, Andrea Scaramuzza, and Carine de Beaufort. Research into Childhood-Onset Diabetes: From Study Design to Improved Management. Springer London, Limited, 2016.

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23

Wilson, John W., and Lynn L. Estes. Sexually Transmitted Diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199797783.003.0121.

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• Abrupt-onset, purulent urethral discharge and dysuria are more common with Neisseria gonorrhoeae than with Chlamydia trachomatis and other nongonococcal urethritis (NGU) pathogens• Mucopurulent or purulent urethral discharge and dysuria, which can occur with any pathogen, often impede clinical distinction• Gram stain of urethral discharge shows >5 leukocytes per high-power field (HPF)...

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24

Mawhorter, Monroe. Hidden Conversation Within Our Bodies: Boost Immunity and Prevent the Onset of Neurological Diseases. Independently Published, 2022.

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25

Grant, William B., and Ronan Lordan, eds. Dietary Patterns, Physical Activity, and Lifestyle in the Onset, Prevention, and Management of Noncommunicable Diseases. MDPI, 2023. http://dx.doi.org/10.3390/books978-3-0365-9551-1.

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26

Jimerson, Shane R., Huijun Li, and Melissa Pearrow. Identifying, Assessing, and Treating Early Onset Schizophrenia at School. Springer, 2012.

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27

Sun, Lisa, and Michael V. Johnston. Rickettsial Diseases. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0157.

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Tick-borne rickettsioses are emerging as more important health problems throughout the world. The spotted fever group including Rickettsia rickettsia can cause encephalopathy, meningitis and brain damage by selectively targeting capillary endothelial cells in the brain, and stimulating inflammation, capillary leakage, hemorrhage, and intravascular coagulation. Rickettsia are are arthropod-borne gram-negative coccobacilli bacteria and are obligate intracellular organisms that do not survive in artificial medium. In North and South America, the most common rickettsial disorder is rocky mountain

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28

Onset of metabolic acidosis (anaerobic threshold) as a criterion measure of submaximum fitness in cardiac rehabilitation patients. 1989.

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29

Shi, Ding, Silvia Turroni, Lan Gong, Wenrui Wu, and Howard Chi Ho Yim, eds. Manipulation of Gut Microbiota as a Key Target to Intervene on the Onset and Progression of Digestive System Diseases. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-181-8.

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Fidaleo, Marco, Franco Scaldaferri, Andrea Quagliariello, and Fausto Andreola, eds. The Role of Microbiota in the Onset and Development of Intestine and Liver Diseases and Cancer: Molecular and Cell Mechanisms. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-805-1.

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31

Ahmed, Ahmed I., Sarah Aldhaheri, and Allison Bannick. Inherited Metabolic Diseases (IMDs) and Pregnancy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0030.

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Inherited metabolic diseases (IMDs) are rare genetic disorders: clinically heterogeneous, and they can present at any age. With the expanded newborn screening panels, many of the IMDs have been successfully screened. Early diagnosis and treatment of these conditions have led to improved neurological outcomes and overall survival of these individuals, and now many of them are reaching childbearing age. Despite treatment, the potential presence of preexisting organ involvement may not only impact their fertility potentials but also may impose a higher risk of adverse maternal and fetal outcomes.

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32

Klaassen, James Kent. Changes in erythrocyte insulin receptors in normal dogs and keeshond dogs with inheritable, early onset, insulin dependent diabetes mellitus. 1986.

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33

Onset of metabolic acidosis (anaerobic threshold) as a criterion measure of submaximum fitness in cardiac rehabilitation patients. 1986.

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34

Onset of metabolic acidosis (anaerobic threshold) as a criterion measure of submaximum fitness in cardiac rehabilitation patients. 1989.

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35

Onset of metabolic acidosis, anaerobic threshold, as a criterion measure of submaximum fitness in cardiac rehabilitation patients. 1989.

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36

Helping People Adapt to the Onset of Psychosis: An Integrated Approach to Recovery. Taylor & Francis Group, 2019.

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37

Jackson, Chris, Mark Bernard, Eleanor Baggott, Ruth Clutterbuck, and Diane Ryles. Helping People Adapt to the Onset of Psychosis: An Integrated Approach to Recovery. Taylor & Francis Group, 2019.

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38

Juvenile Onset Huntington's Disease. MDPI, 2021. http://dx.doi.org/10.3390/books978-3-03943-812-9.

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39

Reading, Paul J. Neurological diseases and their effects on the sleep–wake cycle. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0035.

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This chapter addresses current neurobiological knowledge of how wake- and sleep-promoting systems interact to produce the daily circadian rhythm of wake and sleep and how this may be adversely affected by a variety of neurological diseases. The crucial importance of sleep quality for optimal brain function is stressed and the potential hazards of prolonged wakefulness highlighted. Insomnia relating to either sleep onset or maintenance is common and increases with normal aging. Many neurodegenerative diseases such as Alzheimer disease appear to enhance the effects of aging on the sleep–wake cyc

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40

Barton, Anne. Basics of genetics. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0037.

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Genetic factors are important in predisposing to nearly all of the conditions managed by rheumatologists; indeed, musculoskeletal diseases, like other complex diseases, are thought to be caused by environmental triggers in genetically susceptible individuals. Studying genetic susceptibility factors is more straightforward than environmental factors because, first, genetic changes are stable and do not vary throughout life; second, genetic changes exist before disease onset and so could be causative rather than occurring as a result of disease; and, third, genetic variation is easy to measure r

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41

Zhou, Juan, and William W. Seeley. Brain Circuits. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0007.

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Each neurodegenerative disease is defined by selectively vulnerable neurons, regions, networks, and functions, as well as genetic risk factors. In the past decade, new network-sensitive neuroimaging methods have made it possible to test the notion of network-based degeneration in living humans. This chapter focuses on two common causes of dementia, Alzheimer’s disease (AD) and frontotemporal dementia (FTD), but uses these diseases to illustrate class-wide neurodegeneration principles whenever possible. It first introduces two key concepts of neurodegenerative disease selective vulnerability: o

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42

Tillema, Jan-Mendelt, J. Graves, L. A. Benson, et al. Pediatric Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0022.

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Increased interest in pediatric-onset multiple sclerosis (MS) has contributed to improved knowledge of the presentation and evolution of central nervous system demyelinating diseases in childhood. This chapter reviews the unique features and challenges related to pediatric MS. The close proximity of pediatric MS to the biological onset of the disease provides a unique window into disease pathogenesis at stages of life when innate and adaptive immune pathways are still maturing. It is expected that the interplay between genetics, epigenetics, environmental exposures, and the maturing central ne

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43

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-sympt

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Compston, Alastair. Multiple sclerosis and other demyelinating diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0871.

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The oligodendrocyte–myelin unit subserves saltatory conduction of the nerve impulse in the healthy central nervous system. At one time, many disease processes were thought exclusively to target the structure and function of myelin. Therefore, they were designated ‘demyelinating diseases’. But recent analyses, based mainly on pathological and imaging studies, (re)emphasize that axons are also directly involved in these disorders during both the acute and chronic phases. Another ambiguity is the extent to which these are inflammatory conditions. Here, distinctions should be made between inflamma

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45

Fox, Susan H. Could It Possibly Be … ? Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0027.

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There is increasing recognition of adult presentations of metabolic diseases typically associated with children. These phenotypes are often milder and potentially mistaken for more common adult-onset disorders, therefore requiring a high index of suspicion. The most common adult-onset clinical features involve focal dystonias and parkinsonism. Making a diagnosis of dopa-responsive dystonia in an adult typically involves a therapeutic trial of low-dose levodopa. Genetic testing may be useful to confirm dopa-responsive dystonia and rule out other causes of dystonia and tremor. The neurological e

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46

Leirisalo-Repo, Marjatta, and John D. Carter. Infection and spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0009.

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Spondyloarthritis (SpA) is the designation encompassing a group of inflammatory diseases with several features in common. The patients have mono- or oligoarthritis with or without inflammatory back symptoms. Distinctive extra-articular inflammatory symptoms also characterize the diseases. The diagnostic subgroups in the SpA family include reactive arthritis (ReA), ankylosing spondylitis (AS), arthritis associated with inflammatory bowel disease (IBD), psoriasis arthritis (PsA), and some forms of juvenile-onset arthritis. These diseases share a strong association with a genetic marker, HLA-B27,

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47

Hayduke, John. Adult Onset Still's Disease: A Patient's Perspective. Lulu Press, Inc., 2011.

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48

Struys, Eduard A., Marjo S. van der Knaap, and Gajja S. Salomons. 2-Hydroxyglutaric Acidurias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0022.

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The group of congenital diseases related to 2-hydroxyglutaric acid metabolism consists of five disease entities: D-2-hydroxyglutaric aciduria Type I (D2HGA-I), D-2-hydroxyglutaric aciduria Type II (D2HGA-II), metaphyseal chondromatosis with D-2-hydroxyglutaric aciduria (MC-HGA), L-2-hydroxyglutaric aciduria (L2HGA), and combined D,L-2-hydroxyglutaric aciduria (DL2HGA). Overall, the clinical presentation varies from early onset with mostly lethal neonatal encephalopathy in DL2HGA to slowly progressive mental and motor delay with white matter abnormalities, with an insidious and sometimes adult

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49

Schrifl, Ulrike, SakkuBai Naidu, and Ali Fatemi. Leukodystrophies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0070.

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The term “leukodystrophies” refers to a group of genetic diseases characterized by degeneration of white matter in the central nervous system. Depending on the type of leukodystrophy, the phenotype can range from early infantile-onset, rapid, progressive forms to adult-onset slowly progressive variants. The understanding, definition, and classification have been enhanced greatly by the combined use of neuroimaging, especially MRI, and genetic techniques. The window for targeted therapeutic interventions remains brief and management is often limited to symptomatic, supportive, and palliative ca

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50

Liu, Lena G., and Christina R. Catherine, eds. Women's Neurology. 2nd ed. Oxford University Press, 2025. https://doi.org/10.1093/med/9780197749722.001.0001.

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Abstract This textbook introduces important neurological concepts and disease processes that could potentially affect patients in the antepartum, peripartum or postpartum period, as well as across the lifespan of a woman from puberty to post-menopause. The effect of female hormones (estrogen, progesterone), pregnant state and menopausal state on progression or onset of neurological disease is explored. Emphasis on pregnancy as a state that can improve or worsen symptoms of certain neurological diseases is explored. The importance of pregnancy related diseases such as gestational hypertension o

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