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Готові списки джерел за темами / Disease cycle / Книги

Книги з теми "Disease cycle"

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Disease cycle.

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

Mayerson, Charlotte. The death cycle machine. New York: Crown Publishers, 1995.

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2

Michigan. Department of Community Health. Genetics through the life cycle: Improving health and preventing disease. 8th ed. Lansing, Mich: Michigan Dept. of Community Health, 2004.

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3

Okazawa, T. Biting cycle of malaria vectors in Solomon Islands. Honiara, Solomon Islands: Malaria Training and Medical Centre, Ministry of Health and Medical Services, 1990.

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4

An unbreakable cycle: Drug dependency treatment, mandatory confinement, and HIV/AIDS in China's Guangxi Province. New York, NY: Human Rights Watch, 2008.

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5

1950-, Karmazyn M., Avkiran M, and Fliegel Larry 1956-, eds. The sodium-hydrogen exchanger: From molecule to its role in disease. Boston: Kluwer Academic Publishers, 2003.

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6

Lee, D. ITER safety task NID-10A: CANDU occupational exposure experience : ore for ITER fuel cycle & cooling systems. Mississauga, ON: Canadian Fusion Fuels Technology Project, 1995.

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7

Nawe, Julita. The economic cycle of disease: The case of worker's working conditions with emphasis on women at the Morogoro Leather Goods Co. Ltd., Morogoro, Tanzania. Dar es Salaam [Tanzania]: WRDP, 1990.

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8

Takahashi, Rikiya, and Hibiki Kai. Handbook of macrophages: Life cycle, functions and diseases. Hauppauge, N.Y: Nova Science Publisher's, 2011.

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9

Slade, Suzanne. The Phases of the Moon. New York: Rosen Pub. Group's PowerKids Press, 2007.

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10

Breaking the vicious cycle: Intestinal health through diet. Kirkton, Ontario: Kirkton Press, 1994.

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11

A, Whittington Miles, ed. Cortical oscillations in health and disease. New York: Oxford University Press, 2010.

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12

Traub, Roger D. Cortical oscillations in health and disease. New York: Oxford University Press, 2010.

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13

R, Gluckman Toma, ed. Herpesviridae viral structure, life cycle, and infections. Hauppauge, NY: Nova Science Publishers, 2009.

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14

Blagosklonny, Mikhail V. Cell cycle checkpoints and cancer. Georgetown, Tex: Landes Bioscience, 2001.

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15

Ristow, Sandra S. Research studies on the life cycle of infectious hematopoietic necrosis virus. Portland, OR: U.S. Dept. of Energy, Bonneville Power Administration, Division of Fish and Wildlife, 1990.

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16

Copani, Agata, and F. Nicoletti. Cell-cycle mechanisms and neuronal cell death. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2005.

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17

Tyukavin, Aleksandr. Fundamentals of pathology. ru: INFRA-M Academic Publishing LLC., 2021. http://dx.doi.org/10.12737/1242551.

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Анотація:

The textbook reveals the concepts of health and disease, presents modern ideas about the causes and conditions of the occurrence of actual types of pathology. The importance of molecular genetic factors of heredity and reactivity in the formation of typical pathological processes is shown. The main regularities and features of manifestations of organ and system dysfunction in various types of pathology are described. Special attention is paid to the causes and mechanisms of development of socially significant diseases of the heart and blood vessels, brain, respiratory organs and other vital systems of the body. A separate section of the textbook provides up-to-date information on first aid. The criteria of safe conditions for first aid are described; the main clinical manifestations of emergency conditions in accidents, injuries, poisoning and diseases are described. A list of first aid measures for life-threatening conditions is presented. The cloud service contains a video of the basic algorithm for conducting cardiopulmonary resuscitation in a pharmacy or office. It is written in accordance with the program of the academic discipline "Fundamentals of Pathology" in the specialty 33.02.01 "Pharmacy" and refers to the educational and methodological publications of the cycle of general professional disciplines for students of pharmaceutical technical schools.

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18

Silvio, Gutkind J., ed. Signaling networks and cell cycle control: The molecular basis of cancer and other diseases. Totowa, N.J: Humana Press, 2000.

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19

Yang, Wei Qiang. Blueberry gall midge: A possible new pest in the Northwest : identification, life cycle, and plant injury. [Corvallis, Or.]: Oregon State University Extension Service, 2005.

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20

Mayerson, Charlotte. The Death Cycle Machine. Audio Literature, 1998.

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21

Mayerson, Charlotte. Death Cycle Machine, The. Crown, 1996.

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22

Klink, Professor Dr Joseph-Alexander Verreet and Dr Holger. Potato Late Blight: The Disease Cycle of Phytophthora infestans. Amer Phytopathological Society, 2013.

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23

Ismail, Kareem, and Rabah Arezki. Boom-Bust Cycle, Asymmetrical Fiscal Response and the Dutch Disease. International Monetary Fund, 2010.

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24

Ismail, Kareem, and Rabah Arezki. Boom-Bust Cycle, Asymmetrical Fiscal Response and the Dutch Disease. International Monetary Fund, 2010.

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25

Ismail, Kareem, and Rabah Arezki. Boom-Bust Cycle, Asymmetrical Fiscal Response and the Dutch Disease. International Monetary Fund, 2010.

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26

Plague Cycle: The Unending War Between Humanity and Infectious Disease. Scribner, 2021.

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27

Kenny, Charles. Plague Cycle: The Unending War Between Humanity and Infectious Disease. Scribner, 2021.

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28

Disability, Chronic Disease and Human Development (Pediatrics, Child and Adolescent Health). Nova Science Pub Inc, 2015.

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29

Kenny, Charles. The Plague Cycle: The Unending War Between Humanity and Infectious Disease. Simon & Schuster Audio, 2021.

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30

Kenny, Charles. The Plague Cycle: The Unending War Between Humanity and Infectious Disease. Scribner, 2021.

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31

Veech, Richard L., and M. Todd King. Alzheimer’s Disease. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0026.

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Анотація:

Deficits in cerebral glucose utilization in Alzheimer’s disease (AD) arise decades before cognitive impairment and accumulation of amyloid plaques and neurofibrillary tangles in brain. Addressing this metabolic deficit has greater potential in treating AD than targeting later disease processes – an approach that has failed consistently in the clinic. Cerebral glucose utilization requires numerous enzymes, many of which have been shown to decline in AD. Perhaps the most important is pyruvate dehydrogenase (PDH), which links glycolysis with the Krebs cycle and aerobic metabolism, and whose activity is greatly suppressed in AD. The unique metabolism of ketone bodies allows them to bypass the block at pyruvate dehydrogenase and restore brain metabolism. Recent studies in mouse genetic models of AD and in a human Alzheimer’s patient showed the potential of ketones in maintaining brain energetics and function. Oral ketone bodies might be a promising avenue for treatment of Alzheimer’s disease.

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32

Sugar, David. The disease cycle of side rot of pear, caused by Phialophora malorum. 1989.

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33

Sugar, David. The disease cycle of side rot of pear, caused by Phialophora malorum. 1989.

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34

Kölker, Stefan, Johannes Häberle, and Valerie Walker. Urea Cycle Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0017.

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Анотація:

The urea cycle is the final pathway for removal of surplus nitrogen from the body, the major route in humans for irreversible detoxification of ammonia and a source of arginine.2,3 Patients with adult-onset urea cycle disorders present with clinical symptoms that have a broad differential diagnosis (e.g., protein aversion, inappetence, cyclic vomiting, epilepsy, psychiatric disease, migraine, liver dysfunction). Unlike infants and children some adult-onset patients may never develop acute hyperammonemic crises. Since symptoms are often fluctuating and the diagnosis can only be made if specific tests are made, the diagnosis is often delayed or missed. Earlier detection and intervention would improve the patients’ outcome, which currently is poor.

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35

Chronic Care for Neglected Infectious Diseases: Leprosy/Hansen's Disease, Lymphatic Filariasis, Trachoma, and Chagas Disease. Pan American Health Organization, 2021. http://dx.doi.org/10.37774/9789275122501.

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Анотація:

In 2016, PAHO's Directing Council, through Resolution CD55.R9, approved the “Plan of Action for Elimination of Neglected Infectious Diseases (NID) and Post-Elimination Actions, 2016-2022.” This Resolution urges Member States to implement a set of interventions to reduce the burden of disease by NID in the Americas by 2022, including “…support promotion of treatment, rehabilitation, and related support services through an approach focused on integrated morbidity management and disability prevention for individuals and families afflicted by those neglected infectious diseases that cause disability and generate stigma.” NIDs can have devastating chronic sequelae for patients, such as disability, visible change or loss in body structure, loss of tissue, and impairment of proper tissue and organ function, among others. All of these can in turn lead to unjustified discrimination, stigmatization, mental health problems, and partial or total incapacity to work, perpetuating the vicious cycle of neglected diseases as both a consequence and a cause of poverty. Patients with chronic conditions caused by NIDs require proper health care in order to prevent further damage and improve their living and social conditions. This should be provided at the primary health care level, as patients suffering from NIDs are often unable to travel to or afford to pay for specialized care services. Care for patients suffering from chronic morbidity caused by NID should be integrated into care for other chronic conditions caused by non-communicable diseases. This manual provides a framework for morbidity management and disability prevention of patients affected by NIDs and gives specific guidance for the proper care of patients suffering from chronic conditions caused by lymphatic filariasis, leprosy, trachoma, and Chagas disease. It is intended to be used mainly by health care workers at the primary health care level, but health workers at more complex and specialized levels may also find it useful.

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36

(Editor), Howard J. Federoff, Robert E. Burke (Editor), Stanley Fahn (Editor), and Gary Fiskum (Editor), eds. Parkinson's Disease: The Life Cycle of the Dopamine Neuron (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2004.

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37

Lachmann, Robin, and Elaine Murphy. Aminoacidopathies, urea cycle disorders, and organic acidurias. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0180.

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Aminoacidopathies are caused by deficiencies in enzymes involved in amino acid metabolism and are often characterized by the accumulation of a toxic amino acid. The two diseases most likely to be encountered in adult medicine are phenylketonuria, which is caused by a deficiency of phenylalanine hydroxylase, and maple syrup urine disease (MSUD), which is due to a branched-chain amino acid decarboxylase deficiency. High levels of phenylalanine progressively damage the developing brain, leading to severe learning difficulties. The high levels of leucine which accumulate in MSUD produce an acute encephalopathy which, if not treated, can rapidly become fatal.

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38

Back Sense: A Revolutionary Approach to Halting the Cycle of Chronic Back Pain. Broadway, 2001.

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39

Johnson, D. W. Cankers on western quaking aspen. 1995.

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40

Apoptosis and cell cycle control in cancer: Basic mechanisms and implications for treating malignant disease. Oxford: BIOS Scientific, 1996.

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41

(Editor), Morris Karmazyn, Metin Avkiran (Editor), and Larry Fliegel (Editor), eds. The Sodium-Hydrogen Exchanger: From Molecule to its Role in Disease. Springer, 2003.

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42

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 cycle, with increased fragmentation and reduced deep sleep. Focal pathology in the thalamus or sometimes the hypothalamus may produce striking insomnia, as may several autoimmune encephalitides. Hypersomnia is most often secondary to poor-quality nocturnal sleep, but may also relate to discrete hypothalamic pathology or traumatic head injury. The effects of epilepsy and its treatment on sleep can be significant and are discussed.

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43

H, Lorell Beverly, Grossman William 1940-, and International Symposium on the Biology of Diastole in Health and Disease (1993 : Palm Beach, Fla.), eds. Diastolic relaxation of the heart: The biology of diastole in health and disease. 2nd ed. Boston: Kluwer Academic Publishers, 1994.

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44

(Editor), Beverly H. Lorell, and William Grossman (Editor), eds. Diastolic Relaxation of the Heart: The Biology of Diastole in Health and Disease. 2nd ed. Springer, 2007.

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45

Regulation of Sleep and Circadian Rhythms (Lung Biology in Health and Disease). Informa Healthcare, 1999.

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46

Schofield, C. J. American trypanosomosis (Chagas disease). Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0050.

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Анотація:

American trypanosomosis is due to infection with Trypanosoma cruzi (Protozoa, Kinetoplastidae). This is a widespread parasite of small mammals and marsupials throughout most of the Americas, roughly from the Great Lakes of North America (approx. 42 ° N) to southern Argentina (approx. 46 ° S). It is mainly transmitted by blood-sucking bugs of the subfamily Triatominae (Hemiptera, Reduviidae) which are widespread in the Americas, but rare in the Old World. Except in some research laboratories, and infected immigrants from Latin America, T.cruzi has not been reported from the Old World, although closely-related trypanosome species are commonly found in Old and New World bats.Human infection with T.cruzi is generally known as Chagas disease, taking the name of Brasilian clinician Carlos Justiniano das Chagas who first described it from patients in central Brasil (Chagas 1909). Chagas isolated and described the parasite, correctly deduced most of its life-cycle and clinical symptoms associated with the infection, identified the insect vectors and some of the reservoir hosts, and also trialed initial attempts to control it. He was nominated at least twice for the Nobel prize in medicine (Coutinho and Dias 2000; Lewinsohn 2003).Although difficult to treat, Chagas disease can be controlled by measures to halt transmission, primarily by eliminating domestic populations of the insect vectors, together with serological screening to avoid transmission by blood donation from infected donors. Since 1991, a series of multinational initiatives have used this approach to halt transmission over vast regions of the areas previously endemic for the human infection. Estimated prevalence of the human infection has declined from the 1990 estimate of 16–18 million people infected, to the current estimate of just over 7 million infected (OPS 2006; Schofield & Kabayo 2008). Prevalence is expected to decline further, and control strategies are now being adjusted to develop a sustainable system of disease surveillance, focal vector control, and specific treatment for any new cases (Schofield et al. 2006; WHO 2007). Guidance for diagnosis and treatment is also required for non-endemic countries, where recent years have seen increasing migration from Latin America such that cases of chronic Chagas disease have now been reported from amongst Latin American migrants in Europe, USA and Canada, and Japan, together with some congenital cases and transmission from infected blood donors and by organ transplant.

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47

Rayner, Mike, Kremlin Wickramasinghe, Julianne Williams, Karen McColl, and Shanthi Mendis. Revisiting the stages of the policy cycle. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198791188.003.0015.

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This final chapter argues that the policy cycle should be seen as just that—a cycle, rather than a linear process with a defined start and finish. To generate effective policies, the stages need to be revisited over time. In revisiting these steps, it will be necessary to ask new questions about the problem and the solutions. The chapter includes case studies that illustrate how non-communicable disease (NCD) prevention and control interventions do not always follow the four steps of the policy cycle in a linear process. This chapter emphasizes that NCDs are multifactorial conditions with complex causal webs that require a sophisticated mix of solutions that reflect the specific context. The theoretical background, practical pointers, and case studies from this book should help to equip policy-makers, researchers, health advocates, and students with the knowledge and tools required to reduce the burden of death and disability from NCDs.

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48

(Editor), Howard J. Federoff, Robert E. Burke (Editor), Stanley Fahn (Editor), and Gary Fiskum (Editor), eds. Parkinson's Disease: The Life Cycle of the Dopamine Neuron (Annals of the New York Academy of Sciences, V. 991). New York Academy of Sciences, 2003.

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49

Cavey, J. Possible new introduction-- European spruce bark beetle. 1993.

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50

Lowenthal, A. Urea Cycle Diseases. Springer London, Limited, 2013.

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