Relevant bibliographies by topics / Disease

Academic literature on the topic 'Disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 May 2024

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Journal articles on the topic "Disease":

1

Shanmugam, Sriram, Jaean Kennady, and Jaleel Ahamed. "A CASE STUDY ON WILSON'S DISEASE." International Journal of Medical Reviews and Case Reports 2, Reports in Surgery and Dermatolo (2019): 1. http://dx.doi.org/10.5455/ijmrcr.wilson-disease.

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2

Limpert, E., and P. Bartoš. "Wind-Dispersed Nomadic Diseases: Conclusions for Disease Resistance." Czech Journal of Genetics and Plant Breeding 38, No. 3-4 (August 1, 2012): 150–52. http://dx.doi.org/10.17221/6256-cjgpb.

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3

Dehuri, Priyadarshini, Debasis Gochhait, Debdatta Basu, and Neelaiah Siddaraju. "Rosai-Dorfman Disease: An Imposter of Plasma Cell Rich Diseases." Annals of Pathology and Laboratory Medicine 2, no. 12 (December 17, 2018): C178–181. http://dx.doi.org/10.21276/apalm.2102.

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4

Nakashima, Tsutomu, Koichi Tsuzuki, and Kishiko Sugiyama. "Menière’s Disease or Ménière’s Disease or Meniere’s Disease?" Practica Oto-Rhino-Laryngologica 111, no. 1 (2018): 75–77. http://dx.doi.org/10.5631/jibirin.111.75.

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5

L Pathan, Fayaj. "Nonalcoholic Fatty Liver Disease (NAFLD) A Chronic Liver Disease." Acta Scientifci Nutritional Health 4, no. 1 (December 9, 2019): 58. http://dx.doi.org/10.31080/asnh.2020.04.nonalcoholic-fatty-liver-disease-nafld-a-chronic-liver-disease.

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6

Althaf, Shebin, Manoj Khanal, Anita Rawat, and Kishalay Datta. "Devic’s Disease: The Confusing CNS Disease." Indian Journal of Emergency Medicine 9, no. 3 (September 15, 2023): 107–9. http://dx.doi.org/10.21088/ijem.2395.311x.9323.10.

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Neuromyelitis optica spectrum is order (NMOSD) is a rare auto-antibody mediated disease of the central nervous system involving the central nervous system. The symptoms should alert the clinician to the diagnosis. Prompt diagnosis in the emergency department plays a crucial role as delay in diagnosis and initiation of management will lead to increased chances of morbidity and mortality. Approximately 80% of NMO patients have auto-antibodies against aquaporin-4, a water channel expressed on astrocytes. In this case report, we discuss a patient with NMO disease, the diagnosis and its management.
7

Hananeh, W., and M. Ababneh. "Spotty liver disease in Jordan: An emerging disease." Veterinární Medicína 66, No. 3 (March 2, 2021): 94–98. http://dx.doi.org/10.17221/73/2020-vetmed.

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Spotty liver disease is an acute bacterial disease that affects the poultry industry throughout the world. In this report, we discuss the first documented outbreak of the recently emerging disease, spotty liver disease, in a poultry flock in Jordan. The clinical history, pathological and molecular findings are described. The outbreak was characterised by recurrent mortalities that subsided with antibiotic treatments. Grossly, there were multiple pinpoint white foci distributed throughout the enlarged liver and less frequently throughout the spleen too. Histologically, the white foci represented areas of acute hepatocellular lytic necrosis and degeneration that were consistent with those of spotty liver disease. An end point polymerase chain reaction (PCR) assay targeting the glycerol kinase gene, coupled with sequencing, confirmed the pathological diagnosis. Continuous surveillance is needed to estimate the prevalence of this disease in Jordanian poultry flocks.
8

Verma, Dr Amit Kumar. "Periodontal Disease with Diabetes or Diabetes Kidney Disease." International Journal of Trend in Scientific Research and Development Volume-3, Issue-1 (December 31, 2018): 1043–51. http://dx.doi.org/10.31142/ijtsrd19176.

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9

ITABASHI, Mizuo. "Eponymic Diseases (1): Topics of Takayasu Disease, Hashimoto Disease and Kawasaki Disease." Igaku Toshokan 41, no. 3 (1994): 313–18. http://dx.doi.org/10.7142/igakutoshokan.41.313.

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10

Dassy, Cylia, Manou Saramba, and Dongchi Zhao. "Treatment Options for Complications of Sickle-cell Disease in Children." International Journal of Medical Reviews and Case Reports 4, Reports in Microbiology, Infecti (2020): 1. http://dx.doi.org/10.5455/ijmrcr.sickle-cell-disease-children.

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You might also be interested in the extended bibliographies on the topic 'Disease' for particular source types:
Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Disease":

1

Franco, Iborra Sandra. "Mitochondrial quality control in neurodegenerative diseases: focus on Parkinson’s disease and Huntington’s disease." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/565668.

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Darrerament s’han produït avanços importants que han contribuït al coneixement dels mecanismes de disfunció cel·lular i mort en la malaltia de Parkinson (MP) i en la malaltia de Huntington (MH). Ambdues malalties són trastorns del moviment que es caracteritzen per la pèrdua específica de neurones dels ganglis basals, les neurones dopaminèrgiques de la substància nigra (SN), en el cas de la MP i les neurones espinoses de l’estriat, en el cas de la MH. Malgrat les diferències, ambdues comparteixen processos patològics comuns com la presència de proteïnes malplegades, l’estrés oxidatiu i disfunció mitocondrial. La mitocòndria és la font d’energia principal en les cèl·lules eucariotes, però també és un orgànul dinàmic relacionat amb una gran quantitat de processos cel·lulars. La disrupció de la homeòstasis mitocondrial i la subseqüent disfunció mitocondrial juguen un paper important en la patofisiologia de les malalties neurodegeneratives. El manteniment de la integritat mitocondrial a través de diferents mecanismes de control és crític per a la superviviència neuronal. Aquesta tesi es centra en l’estudi dels mecanismes de control de qualitat mitocondrial en la MP i la MH, per tal d’entendre millor els mecanismes que duen a la mort cel·lular. En el primer capítol, he estudiat el transport de proteïnes a la mitocòndria en models in vitro i in vivo de la MP. In vitro, la inhibició del complexe I produeix una alteració del transport de proteïnes a la mitocòndria així com una disminució dels nivells de proteïnes OXPHOS, acumulació de proteïnes agregades i disminució dels nivells de chaperones mitocondrials. Per tal de restablir el transport de proteïnes mitocondrials es van sobreexpressar dos components clau del sistema de translocases: la translocasa de la membrana externa 20 (TOM20) i la translocasa de la membrana interna 23 (TIM23). La sobreexpressió in vitro de TOM20 i TIM23 va restaurar el transport de proteïnes mitocondrials i va alleugerar la disfunció mitocondrial i la mort cel·lular. La inhibició del complexe I en ratolins també dóna lloc a una alteració del transport de proteïnes mitocondrials i produeix neurodegeneració del sistema dopaminèrgic. La sobreexpressió de TIM23 va restaurar parcialment el transport de proteïnes i va protegir lleugerament les neurones dopaminèrgiques de la SN. En canvi, la sobreexpressió de TOM20 va ser incapaç de millorar el transport de proteïnes mitocondrials i, fins i tot, va exacerbar la mort cel·lular. Aquests resultats posen de relleu el paper de la disfunció del transport de proteïnes mitocondrials, en particular de dos dels seus components, en la patogènesis de la MP i suggereixen la necessitat de futurs estudis es centrin en altres elements d’aquest sistema. En el segon capítol, he estudiat el paper de la proteïna huntingtina en la mitofàgia i com la seva mutació, que dóna lloc a una expansió de glutamines, pot afectar a aquesta funció. Per a tal fi, he treballat en un model in vitro de cèl·lules estriatals ST-Q7 (control) i ST-Q111 (mutant). En condicions fisiològiques, la mitofàgia induïda no es troba mitjançada pel reclutament de parkin als mitocondris despolaritzats. La huntingtina mutada afecta la mitofàgia induïda a través de l’alteració de la seva funció de scaffold en diferents passos del procés de mitofàgia: (i) activació d’ULK1 a través de l’alliberament de mTORC1, (ii) formació del complexe Beclin 1-Vps15,(iii) interacció dels adaptadors de mitofàgia OPTN i NDP52 amb huntingtina i, (iv) amb LC3. Com a resultat, els mitocondris de les cèl·lules ST-Q111 estan més danyats i tenen una respiració mitocondrial deficient. Aquests resultats demostren la presència d’una alteració en la mitofàgia com un mecanisme lligat a la MH. En conclusió, el descobriment de noves dianes mitocondrials en la MP i MH emfatitza el paper important que juga el control de qualitat mitocondrial en la neurodegeneració.
In the past years, several important advances have expanded our understanding of the pathways that lead to cell dysfunction and death in Parkinson’s disease (PD) and Huntington’s disease (HD). Both diseases are movement disorders characterized by the loss of a specific subset of neurons within the basal ganglia, dopaminergic neurons in the substantia nigra pars compacta (SNpc), in the case of PD, and medium spiny neurons in the striatum, in the case of HD,. Despite distinct clinical and pathological features, these two neurodegenerative disorders share critical underlying pathogenic mechanisms such as the presence of misfolded and/or aggregated proteins, oxidative stress and mitochondrial anomalies. Mitochondria are the prime energy source in most eukaryotic cells, but these highly dynamic organelles are also involved in a multitude of cellular events. Disruption of mitochondrial homeostasis and the subsequent mitochondrial dysfunction plays a key role in the pathophysiology of neurodegenerative diseases. Therefore, maintenance of mitochondrial integrity through different surveillance mechanisms is critical for neuronal survival. In this thesis I have studied in depth some mitochondrial quality control mechanisms in the context of PD and HD, in order to broaden the knowledge about the pathomechanisms leading to cell death. In the first chapter I have studied mitochondrial protein import in in vitro and in vivo models of PD. In vitro, complex I inhibition, a characteristic pathological hallmark in PD, impaired mitochondrial protein import. This was associated with OXPHOS protein downregulation, accumulation of aggregated proteins inside mitochondria and downregulation of mitochondrial chaperones. Therefore, we aimed to reestablish the mitochondrial protein import by overexpressing two key components of the system: translocase of the outer membrane 20 (TOM20) and translocase of the inner membrane 23 (TIM23). Overexpression of TOM20 and TIM23 in vitro restored protein import into mitochondria and ameliorated mitochondrial dysfunction and cell death. Complex I inhibition also impaired mitochondrial protein import and led to dopaminergic neurodegeneration in vivo. Overexpression of TIM23 partially rescued protein import into mitochondria and slightly protected dopaminergic neurons in the SNpc. On the contrary, TOM20 overexpression did not rescue protein import into mitochondria and exacerbated neurodegeneration in both SNpc and striatum. These results highlight mitochondrial protein import dysfunction and the distinct role of two of their components in the pathogenesis of PD and suggest the need for future studies to target other elements in the system. In the second chapter, I have studied the role of huntingtin in mitophagy and how the polyglutamine expansion present in mutant huntingtin can affect its function. For such, I worked with differentiated striatal ST-Q7 (as control) and ST-Q111 (as mutant) cells, expressing full length huntingtin. In these conditions, induced mitophagy was not mediated by Parkin recruitment into depolarized mitochondria. Mutant huntingtin impaired induced mitophagy by altering wildtype huntingtin scaffolding activity at different steps of mitophagy process: (i) ULK1 activation through its release from the mTORC1, (ii) Beclin1-Vps15 complex formation, (iii) interaction of the mitophagy adapters OPTN and NDP52 with huntingtin and (iv) with LC3. As a result, mitochondria from ST-Q111 cells exhibited increased damage and altered mitochondrial respiration. These results uncover impaired mitophagy as a potential pathological mechanism linked with HD. In conclusion, we have discovered new mitochondrial targets for PD and HD emphasizing the important role that mitochondrial quality control plays in neurodegeneration
2

Mekaru, Sumiko Rachel. "Environmental risk factors in infectious diseases: studies in waterborne disease outbreaks, Ebola, and Lyme disease." Thesis, Boston University, 2013. https://hdl.handle.net/2144/11144.

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Thesis (Ph.D.)--Boston University
The resurgence of infectious diseases and global climate change's potential impact on them has refocused public health's attention on the environment's role in infectious disease. The studies in this dissertation utilize the increased availability of satellite image-derived data sets with fine temporal and geographic granularity and the expansion of epidemiologic methods to explore the relationship between the environment and infectious disease in three settings. The first study employed a novel study design and analytic methods to investigate the hypothesis that heavy rainfall is an independent risk factor for waterborne disease outbreaks (WBDOs). We found that a location experiencing a heavy rainfall event had about half the odds of a WBDO two or four weeks later than did a location without a heavy rainfall event. The location-based case-crossover study design utilized in this study may help to expand the research methods available to epidemiologists working in this developing field. The second study employed a location-based case-crossover study design to evaluate standardized differences from historic average of weekly rainfall in locations with a recorded introduction of Ebola into a human. For each 1.0 unit z-score decrease in total rainfall, the odds of an Ebola introduction three weeks later increased by 75%. Given the severity of Ebola outbreaks and the dearth of knowledge about indicators of increased risk, this finding is an important step in advancing our understanding of Ebola ecology. The third study used GIS methods on remote sensing data to estimate the association between peridomestic forest/non-forest interface within 100, 150, 250 meters and Lyme-associated peripheral facial palsy (LAPFP) among pediatric facial palsy patients. After adjustment for sex, age, and socio-economic status, children with the highest level of forest edge in the three radii of analysis had 2.74 (95% CI 1.15, 6.53), 4.58 (1.84, 11.41), and 5.88 (2.11, 16.4) times the odds of LAPFP compared to children with zero forest edge in those radii. This study is the first to examine environmental risk factors for LAPFP. Each of these studies advances the techniques used to investigate environmental risk factors for infectious disease through study design, case definition, data used, or exposure definitions.
3

Pietravalle, Stéphane. "Modelling weather/disease relationships in winter wheat diseases." Thesis, University of Reading, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402602.

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4

Haslam, Bryan (Bryan Todd). "Learning diseases from data : a disease space odyssey." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/114002.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, 2017.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 253-280).
Recent commitments to enhance the use of data for learning in medicine provide the opportunity to apply instruments and abstractions from computational learning theory to systematize learning in medicine. The hope is to accelerate the rate at which we incorporate knowledge and improve healthcare quality. In this thesis, we work to bring further clarity to the ways in which computational learning theory can be applied to update the collective knowledge about diseases. Researchers continually study and learn about the complex nature of the human body. They summarize this knowledge with the best possible set of diseases and how those diseases relate to each other. We draw on computational learning theory to understand and broaden this form of collective learning. This mode of collective learning is regarded as unsupervised learning, as no disease labels are initially available. In unsupervised learning, variance is typically reduced to find an optimal function to organize the data. A significant challenge that remains is how to measure variance in the definition of diseases in a comprehensive way. Variance in the definition of a disease introduces a systematic error in both basic and clinical research. If measured, it would also be possible to use computers to efficiently minimize variance, providing a great opportunity for learning by utilizing medical data. In this thesis, we demonstrate that it is possible to estimate variance in the disease taxonomy, effectively estimating an error bar for the current definitions of diseases. We do so using the history of the disease taxonomy and comparing it with a variety of external data sets that relate diseases to attributes such as symptoms, drugs and genes. We demonstrate that variance can be significant over relatively short time periods. We further present methods for updating the disease taxonomy by reducing variance based on external disease data sets. This makes it possible to automatically incorporate information contained in disease data sets into the disease taxonomy. The approach also makes it possible to use expert information encoded in the taxonomy to systematically transfer knowledge and update other biomedical data sets that are often sparse (e.g. - symptoms associated with diseases). A natural question stemming from these results is how granular does data need to be to make improvements? For instance, is patient-level data necessary to enable learning at the macro level of disease? Or are there strategies to extract information from other kinds of data to alleviate the need for very granular data. We show that detailed, patient-level data is not necessarily needed to extract detailed biological data. We do so by comparing disease relationships learned from clinical trial metadata to disease relationships learned from a detailed genetic database and show we can achieve similar results. This result shows that we can use currently available data and take advantage of computational learning to improve disease learning, which suggests a new avenue to improving patient outcomes. By reducing variance within diseases using data available today, we can quickly update the space of diseases to be more precise. Precise diseases lead to better learning in other areas of medicine and ultimately improved healthcare quality.
by Bryan Haslam.
Ph. D.
5

Guallar-Hoyas, Cristina. "Prospecting for markers of disease in respiratory diseases." Thesis, Loughborough University, 2013. https://dspace.lboro.ac.uk/2134/12415.

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Asthma, current detection methods and metabolites proposed as asthma markers are described. The limitation of the disease diagnosis is outlined and metabolomics is introduced as the approach carried out within this research with the potential to measure the group metabolites that characterise the metabolic responses of a biological system to a specific disease. Chemistry underlying breathing, current breath collection and analytical techniques are described as well as detection and data processing technology associated within our research. A work-flow for the collection, analysis and processing of exhaled breath samples in respiratory diseases is described. The non-invasive sampling method allows collection of exhaled breath samples on children and adults without experiencing any discomfort. The analysis of exhaled breath samples using thermal desorption gas chromatography mass spectrometry outlines the use of retention index for the alignment of VOCs retention time shifting over time. This methodology enables the creation of a breath matrix for multivariate analysis data processing where each VOC is defined by retention index and most intense fragments of the mass spectrum. This methodology is tested in two cohorts of participants: paediatric asthma and severe asthmatic participants whose breath profiles are compared against healthy controls and within the two asthmatic phenotypes to prospect the markers that differentiate between the different groups. Eight candidate markers are identified to discriminate between asthmatic children and healthy children and seven markers between asthmatics undergoing therapy and healthy controls. The database from severe and paediatric asthma is compared, establishing seven non-age related markers between the two groups. A new interface is developed for the faster analysis of exhaled breath samples using thermal desorption ion mobility mass spectrometry. The interface front end has been modified and optimised to achieve the best sensitivity and resolution of VOCs in exhaled breath. A preliminary study carried out in a small cohort of volunteers shows the feasibility of the technique for the differentiation of asthmatic and healthy adults.
6

George, Charles Raymond Pax. "Disease Explicated And Disease Defined." Thesis, The University of Sydney, 2005. http://hdl.handle.net/2123/654.

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Disease is ubiquitous. Disease afflicts humans. It afflicts animals. It afflicts plants. People refer to disease in their everyday conversation. Newspapers comment upon it. Parliaments enact legislation regarding it. Novelists write about it. Artists depict it. Physicians, veterinary surgeons and agriculturalists seek to combat it. Insurance companies offer reimbursement against it. Anthropologists study it. Philosophers debate its nature, and dictionaries define it. Disease looms large in human consciousness. One might presume that, since disease is so important in daily life, human beings would know exactly what they mean by it. Most people seem to believe instinctively that they understand the nature of disease, and that their ideas about it coincide with other people's ideas. The definition of disease therefore arouses little controversy in everyday conversation. People use the word disease as readily as they use the words spade, or table or nose. They suggest, when they joke that somebody calls a spade a spade, that the nature of the implement used to dig the garden is so obvious that it requires no further definition. Similarly with a table or a nose. They might debate how many legs a table must have, but-regardless of the answer-rarely deny that it is a table; whilst every human must surely know what a nose is. This high level of agreement about so many commonly used terms perhaps creates an assumption that the meaning of disease is equally obvious and requires no further analysis. Is this, however, really the case? Disease is a somewhat less concrete phenomenon than is a spade or a table or a nose. Its existence, most would agree, is incontrovertible, but its nature is less clear. It is something that seems to befall people and animals and plants. It rarely serves any useful purpose. It often carries dire implications. It is something that most of us would prefer not to have, but rarely succeed in avoiding. It commonly comes unannounced and at inconvenient times. It usually causes distress, but not always. It can have a fatal outcome. Some people appear more prone to it that others. It sometimes sweeps through whole populations producing social devastation, but its manifestations vary. Some diseases affect a person's whole body, others merely a part of the body; some affect some parts of the body, others other parts. Some diseases only affect humans, whereas others affect both humans and animals. Some spread from animals to humans, others from humans to humans, and others still do not appear to spread at all. Some diseases affect plants, and few that affect plants seem to affect humans, but some humans can acquire diseases when they come into contact with plants that appear to have no diseases. Any reasonable analysis of the nature of disease must account for all these aspects and many others also. The nature of disease is a topic that has attracted the attention of physicians, scientists and philosophers over millennia. The close association that existed between medicine and philosophy in the classical Egyptian, Palestinian and Greek eras ensured that scholars who flourished in those societies examined the nature of disease. Comparable developments occurred in classical Indian and Chinese civilizations. The natural philosophers of Renaissance and post-Renaissance Europe divided into competing schools of thought over the nature of disease. More recent years have witnessed an enormous flourishing of physicians, pathologists, and agriculturalists who study aspects of disease that relate to their individual disciplines. Most of these researchers have, however, examined ever-narrower aspects of specific diseases-such as manifestations, mechanisms and causes-rather than the generic nature of the phenomenon. Some contemporary philosophers, on the other hand, have become interested in general aspects of the topic. They have proposed a number of novel ideas and reached some stimulating conclusions, although they can hardly yet claim to have reached a consensus. This lack of unanimity presumably implies that the issues involved require closer analysis if a formulation is to emerge that most of them can accept. The object of the present thesis is to undertake such an analysis. It will start by outlining in this introduction the general background to the topic. It will then detail the more noteworthy of previously proposed theories about the nature of this phenomenon, classifying them according to their most prominent components, and assessing their several strengths and weaknesses. It will next discuss the specific philosophical issues of definition, causation, and explication in the biomedical context, before suggesting a comprehensive, but succinct, definition that acknowledges many older views about disease, encompasses current usage, and provides a theoretical base from which to work into the future. It will finally test the strengths and weaknesses of that definition to account for observed phenomena and to accommodate some former definitions.
7

George, Charles Raymond Pax. "Disease Explicated And Disease Defined." University of Sydney. History and Philosophy of Science, 2005. http://hdl.handle.net/2123/654.

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Abstract:
Disease is ubiquitous. Disease afflicts humans. It afflicts animals. It afflicts plants. People refer to disease in their everyday conversation. Newspapers comment upon it. Parliaments enact legislation regarding it. Novelists write about it. Artists depict it. Physicians, veterinary surgeons and agriculturalists seek to combat it. Insurance companies offer reimbursement against it. Anthropologists study it. Philosophers debate its nature, and dictionaries define it. Disease looms large in human consciousness. One might presume that, since disease is so important in daily life, human beings would know exactly what they mean by it. Most people seem to believe instinctively that they understand the nature of disease, and that their ideas about it coincide with other people�s ideas. The definition of disease therefore arouses little controversy in everyday conversation. People use the word disease as readily as they use the words spade, or table or nose. They suggest, when they joke that somebody calls a spade a spade, that the nature of the implement used to dig the garden is so obvious that it requires no further definition. Similarly with a table or a nose. They might debate how many legs a table must have, but�regardless of the answer�rarely deny that it is a table; whilst every human must surely know what a nose is. This high level of agreement about so many commonly used terms perhaps creates an assumption that the meaning of disease is equally obvious and requires no further analysis. Is this, however, really the case? Disease is a somewhat less concrete phenomenon than is a spade or a table or a nose. Its existence, most would agree, is incontrovertible, but its nature is less clear. It is something that seems to befall people and animals and plants. It rarely serves any useful purpose. It often carries dire implications. It is something that most of us would prefer not to have, but rarely succeed in avoiding. It commonly comes unannounced and at inconvenient times. It usually causes distress, but not always. It can have a fatal outcome. Some people appear more prone to it that others. It sometimes sweeps through whole populations producing social devastation, but its manifestations vary. Some diseases affect a person�s whole body, others merely a part of the body; some affect some parts of the body, others other parts. Some diseases only affect humans, whereas others affect both humans and animals. Some spread from animals to humans, others from humans to humans, and others still do not appear to spread at all. Some diseases affect plants, and few that affect plants seem to affect humans, but some humans can acquire diseases when they come into contact with plants that appear to have no diseases. Any reasonable analysis of the nature of disease must account for all these aspects and many others also. The nature of disease is a topic that has attracted the attention of physicians, scientists and philosophers over millennia. The close association that existed between medicine and philosophy in the classical Egyptian, Palestinian and Greek eras ensured that scholars who flourished in those societies examined the nature of disease. Comparable developments occurred in classical Indian and Chinese civilizations. The natural philosophers of Renaissance and post-Renaissance Europe divided into competing schools of thought over the nature of disease. More recent years have witnessed an enormous flourishing of physicians, pathologists, and agriculturalists who study aspects of disease that relate to their individual disciplines. Most of these researchers have, however, examined ever-narrower aspects of specific diseases�such as manifestations, mechanisms and causes�rather than the generic nature of the phenomenon. Some contemporary philosophers, on the other hand, have become interested in general aspects of the topic. They have proposed a number of novel ideas and reached some stimulating conclusions, although they can hardly yet claim to have reached a consensus. This lack of unanimity presumably implies that the issues involved require closer analysis if a formulation is to emerge that most of them can accept. The object of the present thesis is to undertake such an analysis. It will start by outlining in this introduction the general background to the topic. It will then detail the more noteworthy of previously proposed theories about the nature of this phenomenon, classifying them according to their most prominent components, and assessing their several strengths and weaknesses. It will next discuss the specific philosophical issues of definition, causation, and explication in the biomedical context, before suggesting a comprehensive, but succinct, definition that acknowledges many older views about disease, encompasses current usage, and provides a theoretical base from which to work into the future. It will finally test the strengths and weaknesses of that definition to account for observed phenomena and to accommodate some former definitions.
8

Gu, Mei. "Mitochondrial function in Parkinson's disease and other neurodegenerative diseases." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322371.

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9

Ullah, Naseem. "Disease modules identification in heterogenous diseases with WGCNA method." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-16692.

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The widely collected and analyzed genetic data help in understanding the underlying mechanisms of heterogeneous diseases. Cellular components interact in a network fashion where genes are nodes and edges are the interactions. The failure in individual genes lead to dys-regulation of sub-groups of genes which causes a disease phenotype, and this dys-functional region is called a disease module. Disease module identification in complex diseases such as asthma and cancer is a huge challenge. Despite the development of numerous sophisticated methods there is a still no gold standard. In this study we apply different parameter settings to test the performance of a widely used method for disease module detection in multi-omics data called Weighted Gene Co-expression Network Analysis (WGCNA). A systematic approach is used to identify disease modules in asthma and arthritis diseases. The accuracy of obtained modules is validated by a pathway scoring algorithm (PASCAL) and GWAS SNP enrichment. Our results differ between the tested data sets and therefore we cannot conclude with recommendations for an optimal setting that could perform best for multiple data sets using this method.
10

Mancini, Sabrina. "Assessment of a screening test for MMP-8 activity in the diagnosis of periodontal diseases." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0028/MQ40755.pdf.

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Books on the topic "Disease":

1

Edward, Willett. Disease-hunting scientist: Careers hunting deadly diseases. Berkeley Heights, NJ: Enslow, 2009.

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2

Filer, Joyce. Disease. London, UK: British Museum Press, 1995.

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3

Filer, Joyce. Disease. Austin: University of Texas Press, 1996.

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Ridley, Matt. Disease. London: Phoenix, 1997.

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1943-, Stein Mark R., ed. Gastroesophageal reflux disease and airway disease. New York: Marcel Dekker, 1999.

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Mulder, Chris J. J., and Guido N. J. Tytgat, eds. Is Crohn’s Disease a Mycobacterial Disease? Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-1830-9.

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Willett, Edward. Infectious disease specialists: Hunting down disease. New York: Enslow Publishing, 2016.

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J, Mulder C. J., and Tytgat G. N. J, eds. Is Crohn's disease a mycobacterial disease? Dordrecht: Kluwer Academic Publishers, 1992.

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LLC, National Health Information, ed. Heart disease: Disease management strategies & programs. Atlanta, GA: National Health Information, 2005.

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R, Nichols, ed. Mycoplasma diseases of ruminants: Disease, diagnosis and control. Wallingford: CABI, 2006.

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Book chapters on the topic "Disease":

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Weis, Serge, Michael Sonnberger, Andreas Dunzinger, Eva Voglmayr, Martin Aichholzer, Raimund Kleiser, and Peter Strasser. "Neurodegenerative Diseases: Parkinson Disease." In Imaging Brain Diseases, 1001–20. Vienna: Springer Vienna, 2019. http://dx.doi.org/10.1007/978-3-7091-1544-2_37.

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Weis, Serge, Michael Sonnberger, Andreas Dunzinger, Eva Voglmayr, Martin Aichholzer, Raimund Kleiser, and Peter Strasser. "Neurodegenerative Diseases: Huntington Disease." In Imaging Brain Diseases, 1059–68. Vienna: Springer Vienna, 2019. http://dx.doi.org/10.1007/978-3-7091-1544-2_40.

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Gregori, Maria, and Francesca Re. "Neurodegenerative Diseases - Alzheimer's Disease." In Pharmaceutical Nanotechnology: Innovation and Production, 649–60. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2016. http://dx.doi.org/10.1002/9783527800681.ch27.

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Tamma, Filippo. "Extrapyramidal Diseases: Parkinson’s Disease." In Prognosis of Neurological Diseases, 363–68. Milano: Springer Milan, 2015. http://dx.doi.org/10.1007/978-88-470-5755-5_28.

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Valzania, Franco. "Extrapyramidal Diseases: Huntington’s Disease." In Prognosis of Neurological Diseases, 375–79. Milano: Springer Milan, 2015. http://dx.doi.org/10.1007/978-88-470-5755-5_30.

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Kenanidis, Eustathios, Andreas Leonidou, Michael Potoupnis, Eleftherios Tsiridis, Aristotelis Kourtis, and Richard P. Baker. "Neurologic Diseases: Parkinson’s Disease." In The Adult Hip - Master Case Series and Techniques, 327–37. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-64177-5_11.

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Muñoz, Melissa, Elizabeth Cieniewicz, and James E. Faust. "Diseases and disease management." In Cut flowers and foliages, 258–315. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781789247602.0006.

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Abstract:
Abstract This chapter describes the general principles of disease management that apply to all pathogens, followed by a detailed description of the major pathogens, which fall into 4 broad categories, i.e. fungi/oomycetes, bacteria/phytoplasma, viruses and nematodes. The most important diseases of cut flowers, their causal microorganisms, symptoms and signs, epidemiology and management practices are addressed and organized by the primary tissues affected.
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Weis, Serge, Michael Sonnberger, Andreas Dunzinger, Eva Voglmayr, Martin Aichholzer, Raimund Kleiser, and Peter Strasser. "Neurodegenerative Diseases: Alzheimer Disease (AD)." In Imaging Brain Diseases, 897–931. Vienna: Springer Vienna, 2019. http://dx.doi.org/10.1007/978-3-7091-1544-2_32.

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Kanki, Phyllis J. "Infectious Diseases infectious disease , Introduction." In Encyclopedia of Sustainability Science and Technology, 5378–82. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0851-3_927.

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Chen, Yen-Ping, Chao-Fang Yu, and Yu-Hua Shih. "Duck Diseases and Disease Management." In Duck Production and Management Strategies, 549–79. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-6100-6_14.

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Conference papers on the topic "Disease":

1

Collar, Giovanna Carello, Marco Antônio De Bastiani, and Eduardo R. Zimmer. "HUNTINGTON’S DISEASE AND EARLYONSET ALZHEIMER’S DISEASE SHARE A TRANSCRIPTOMIC SIGNATURE." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda082.

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Background: Neurodegenerative diseases share progressive loss of neurons and protein misfolding, which ultimately culminates in dementia; many diseases have been identified as causes of early-onset dementia (< 65 years of age) such as Huntington’s disease (HD) and early-onset Alzheimer’s disease (EOAD). Importantly, disease-specific genetic mutations have already been identified for HD and EOAD. Thus, one could suggest that the molecular link between these diseases may arise from alterations at the transcriptomic level, which is yet to be determined. Objective: We aimed at identifying transcriptome similarities between HD and EOAD. Methods: We collected data of the postmortem cerebral cortex from 1 HD and 6 AD microarray studies in the Gene Expression Omnibus. Of note, only subjects with age at death under 65 were selected (HD: n = 158, controls: n = 158; EOAD: n = 65, controls: n = 266). Differential expression and functional enrichment analyses were performed. Results: We identified 1,260 differentially expressed genes and 675 enriched gene ontology terms between HD and EOAD. Conclusion: Our results demonstrate a transcriptomic signature shared by HD and EOAD. Unveiling the similarities between these diseases at the transcriptomic level could advance our knowledge about pathogenesis and may help to develop therapeutic strategies targeting early-onset dementias.
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HELIALDO SOUSA DE OLIVEIRA FILHO, FRANCISCO, PRISCILA DOURADO EVANGELISTA, PRISCILA GARCIA CÂMARA CABRAL TAVARES, LUIZ VALÉRIO COSTA VASCONCELOS, MARINA PINTO ROCHA, ANA CAROLINA CAVALCANTE MENDONÇA, ADAH SOPHIA RODRIGUES VIEIRA, et al. "LEPROSY: INFECTIOUS DISEASE MIMICKING RHEUMATIC DISEASES." In SBR 2021 Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2021.1806.

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Gómez, Carlota, Irene Jimeno, Leonardo De la Torre, and Monika Wozniak. "VISIBILIZING INVISIBLE DISEASES: FACE CHAGAS DISEASE." In 11th International Conference on Education and New Learning Technologies. IATED, 2019. http://dx.doi.org/10.21125/edulearn.2019.0932.

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"Skin Disease Classification Using Deep Learning CNN." In The International Conference on scientific innovations in Science, Technology, and Management. International Journal of Advanced Trends in Engineering and Management, 2023. http://dx.doi.org/10.59544/ngnt7820/ngcesi23p151.

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Skin disease is one of the large numbers of spread diseases in the world. Its diagnoses are very difficult because of its difficulties in the skin texture, presence of hair on skin and colour. Thus, it is required to develop an efficient method for the diagnosis of skin disease based on deep learning in order to increase the accuracy of diagnosis for different skin types. Now a days, deep learning techniques are more popular in medical diagnosis system. This work focuses on skin disease prediction using deep learning technique. For the implementation, the dataset used for the skin disease prediction is the ISIC dataset with 9 category of skin diseases. For the classification, the deep learning algorithm used is Visual Geometry Group 19 (VGG 19). VGG 19 is a pretrained neural network, which can be used for the detection of skin disease detection using the concept of transfer learning. For that the neural network extracts image features from the skin images. The extracted features are used for the detection of skin disease within the 7 classes of skin diseases.
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P., Deepthi, Dhinakaran M., and Yoganapriya R. "Fruit Disease Detection Using Image Processing." In The International Conference on scientific innovations in Science, Technology, and Management. International Journal of Advanced Trends in Engineering and Management, 2023. http://dx.doi.org/10.59544/bfbm3617/ngcesi23p87.

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Nowadays, production of mango fruit decreases because of climatic conditions and environmental concerns like heavy rain, high humidity, reduction in soil nutrients, diversity of associated diseases and disorder problems. Typically, the detection of mango Plant diseases is done by naked eye observation, which provides less accuracy. Low productivity of mango fruit is due to the various diseases affecting mango plants which are not recognized by the farmers as they are illiterate. This paper holds a survey on fruit disease detection using image processing techniques. DIP is a fast and accurate technique for detection of diseases in fruits. Identification and classification of diseases of fruits are done through various algorithms. This paper is fruit disease identification and classification techniques used by different authors. Techniques include clustering and CBS, ANN and different classifiers-based classification of diseases. The main focus of our work is obtaining the analysis of different fruit diseases detection techniques and also provides an overview of these techniques. All the work is done using Python and supporting libraries.
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Sandeep Kumar, S., and Usha Divakarla. "Mulberry Leaves Diseases and Disease Identification Techniques." In 2023 International Conference on Integrated Intelligence and Communication Systems (ICIICS). IEEE, 2023. http://dx.doi.org/10.1109/iciics59993.2023.10421635.

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Guelli, Mariana Sandoval Terra Campos, Daniela Bastos de Almeida Zampier, Lorena Araújo Silva Dias, and Marina de Oliveira Nunes Ibrahim. "Creutzfeldt-Jakob Disease - a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.126.

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Background: Creutzfeldt-Jakob disease (CJD) is a progressive, rare, fatal and rapid human neurodegenerative disease that occurs in the etiologies: sporadic (CJD), familial, iatrogenic (CJD) and CJD variant (CJV) in which cell prion protein (PrP) can be transmitted through animals. Objectives: Literature review about Creutzfeldt-Jakob diseaseDesign and setting: Literature review development in the Centro Universitário de Volta Redonda, Rio de Janeiro, Brazil. Methods: The Creutzfeldt-Jakob disease, infectious diseases and neuroinfection indexes were used in the PUBMED and Scielo databases. Results:CJD has different etiologies with different clinical and pathological phenotypes. CJDV shows psychiatric behaviors and symptoms followed by abnormalities, ataxia and dementia. The sporadic form is the most common, with a progressive clinical course with generalized brain deposition of abnormal prion protein aggregates (PrPTSE) that leads to spongiform change, gliosis and neuronal loss. CJD progresses to dementia and two or more symptoms: cerebellar or visual impairments; pyramidal or extrapyramidal signs; myoclonus; and akinetic mutism. Complex periods of acute wave in the electroencephalogram (EEG) are strongly suggestive of prionic diseases. Rapidly evolving field neuroimmune disorders have shown an increasing in autoantibody testing; attempt to diagnose a range of immune-mediated conditions. Evidence indicates that diffusion-weighted magnetic resonance imaging (DWI) is more sensitive for detecting signal abnormalities. Conclusion: The disease progresses to dementia, accompanied by myoclonus, pyramidal signs and characteristic EEG. It is a complex pathology, which has only symptomatic treatment and requires strict control of reservoirs and risk of contamination.
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Greenstein, Vivienne C., and Donald C. Hood. "A Test of the Decreased Responsiveness Hypothesis in Retinitis Pigmentosa." In Noninvasive Assessment of Visual Function. Washington, D.C.: Optica Publishing Group, 1985. http://dx.doi.org/10.1364/navf.1985.tua2.

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The most fundamental deficit attributable to retinal disease is a reduction in sensitivity to light. Recently we suggested a simple physiological basis for this sensitivity loss (Hood and Greenstein, 1982, Greenstein et al., 1982.). Based upon psychophysical experiments performed on patients with a variety of retinal diseases we hypothesized that in the diseased retina all retinal cells are less responsive to light. That is because of anoxia, or decreased metabolic activity, or some other factor, retinal cells respond to all light intensities with a fraction of the response produced in a non-diseased retina. In fact, much of our data suggest that a simple form of this explanation can be applied to the retinal diseases we studied. It is not surprising that decreased cellular responsiveness occurs in a disease like diabetic retinopathy; it is surprising that the loss in foveal sensitivity found in a group of patients with retinitis pigmentosa (RP) was consistent with this explanation (Greenstein et al. 1984). If sensitivity loss in RP can be attributed entirely to decreased responsiveness then the effects of adding adapting lights are quantitatively predictable. In this paper this hypothesis is tested by collecting foveal data at two levels of steady adaptation on a selected group of RP patients.
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Vedika, R., M. Mithra Lakshmi, R. Sakthia, and K. Meenakshi. "Early Wheat Leaf Disease Detection Using CNN." In International Research Conference on IOT, Cloud and Data Science. Switzerland: Trans Tech Publications Ltd, 2023. http://dx.doi.org/10.4028/p-653bh6.

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Smart farming is an innovative technology that aids in the improvement of the country's agricultural produce quality and quantity. Wheat is the most important crop in most parts of India. Wheat leaf diseases have a significant impact on production rates and farmer earnings. It poses a significant danger to food security because it affects crop productivity and degrades crop quality. Accurate and precise disease detection has posed a significant challenge, but recent advances in computer vision enabled by deep learning have paved the road for camera-assisted wheat leaf disease diagnosis. Using a CNN trained with a publicly available wheat leaf disease model, several machine learning algorithms and neuron- and layer-wise visualization methods are applied.
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Colombel, Jean-Frederic, and Karin Drooff. "CD: Induction treatment with upadacitinib successful in clinical and endoscopic ratings." In Digestive Disease Week 2022, edited by Rachel Giles. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/13ea239a.

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Reports on the topic "Disease":

1

Del Valle, Sara. Disease Precognition. Office of Scientific and Technical Information (OSTI), August 2021. http://dx.doi.org/10.2172/1812633.

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Oster, Emily. Does Disease Cause Vaccination? Disease Outbreaks and Vaccination Response. Cambridge, MA: National Bureau of Economic Research, July 2016. http://dx.doi.org/10.3386/w22464.

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Zhao, Junyu, Yutian Tian, Haipeng Wang, Jinming Yao, Wang Song, and Yaru Mou. Thyroid diseases are associated with coronavirus disease 2019 (COVID-19) infection. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2021. http://dx.doi.org/10.37766/inplasy2021.9.0079.

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Evans, Celia A., Jennifer A. Lucas, and Mark J. Twery. Beech Bark Disease: Proceedings of the Beech Bark Disease Symposium. Newtown Square, PA: U.S. Department of Agriculture, Forest Service, Northeastern Research Station, 2005. http://dx.doi.org/10.2737/ne-gtr-331.

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Li, Jiawang, Xiangyun Chen, Hongrui Zhang, Wei Ding, Danni Chen, Ning Liang, Haiying Tong, Zhenhong Liu, and Zhen Yang. A Systematic Review of the Capsaicin and other TRPV1 agonists effects on three neurodegenerative diseases: Alzheimer's disease, Parkinson's disease and Ischemic Stroke. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2024. http://dx.doi.org/10.37766/inplasy2024.4.0115.

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Kostoff, Ronald N. Literature-Related Discovery: Common Factors for Parkinson's Disease and Crohn's Disease. Fort Belvoir, VA: Defense Technical Information Center, January 2010. http://dx.doi.org/10.21236/ada525269.

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Somerville, Shauna C. Powdery Mildew Disease Resistance. Office of Scientific and Technical Information (OSTI), August 2010. http://dx.doi.org/10.2172/1123169.

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Pellegrino, Bruno, and Luigi Zingales. Diagnosing the Italian Disease. Cambridge, MA: National Bureau of Economic Research, October 2017. http://dx.doi.org/10.3386/w23964.

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Licht, Mark A., and Wayne B. Roush. Insects and Disease Update. Ames: Iowa State University, Digital Repository, 2010. http://dx.doi.org/10.31274/farmprogressreports-180814-112.

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Licht, Mark A., Joel L. DeJong, and Wayne B. Roush. Insects and Disease Update. Ames: Iowa State University, Digital Repository, 2011. http://dx.doi.org/10.31274/farmprogressreports-180814-1248.

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