Relevant bibliographies by topics / Diseases

Academic literature on the topic 'Diseases'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 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 "Diseases":

1

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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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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Balaji, SM. "Noncommunicable diseases and dental diseases." Indian Journal of Dental Research 29, no. 6 (2018): 699. http://dx.doi.org/10.4103/ijdr.ijdr_895_18.

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Heinz, Don J., and Steve A. Ferreira. "Diseases of sugarcane. Major diseases." Field Crops Research 19, no. 1 (August 1988): 77–78. http://dx.doi.org/10.1016/0378-4290(88)90037-8.

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Kadirovna, Muratova Saodat, Shukurova Nodira Tillayevna, Baratov Bobur, and Teshayev Shoxjahon. "PREDICTIVE MODELING OF THE PROBABILITY OF DEVELOPING PERIODONTAL DISEASES IN PATIENTS WITH CARDIOVASCULAR DISEASE." European International Journal of Multidisciplinary Research and Management Studies 4, no. 4 (April 1, 2024): 65–70. http://dx.doi.org/10.55640/eijmrms-04-04-10.

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Currently, the forecast of the development of pathology is an important part of all branches of healthcare. [3,4,5]. However, despite the importance and scientific and practical significance of forecasting in dentistry, at present we have not found information about predictive models of individual risk of developing periodontitis in patients with hypertension.
6

MATSUMOTO, KEIZO. "Emerging infectious diseases and insensible bacillus infectious diseases. Emerging infectious diseases. Influenza virus infection diseases." Nihon Naika Gakkai Zasshi 86, no. 11 (1997): 2033–38. http://dx.doi.org/10.2169/naika.86.2033.

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&NA;. "Diseases." Inpharma Weekly &NA;, no. 872 (January 1993): 5. http://dx.doi.org/10.2165/00128413-199308720-00007.

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Kumagai, Shunichi. "7. Collagen Diseases and Allergic Diseases." Nihon Naika Gakkai Zasshi 97, no. 12 (2008): 2991–97. http://dx.doi.org/10.2169/naika.97.2991.

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Tatsumi, Koichiro. "Respiratory diseases as lifestyle-related diseases." Health Evaluation and Promotion 39, no. 6 (2012): 821–28. http://dx.doi.org/10.7143/jhep.39.821.

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Arma, Utmi, and Nadhifah Salsabila. "Peri-Implant Diseases and Gastrointestinal Diseases." Archives of Orofacial Sciences 16, Supp. 1 (September 22, 2021): 1–4. http://dx.doi.org/10.21315/aos2021.16.s1.1.

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Peri-implant diseases are serious problems that plagues today’s dentistry, both in terms of therapy and epidemiology. With the expansion of implantology practice and the increasing number of implants placed annually, the frequency of peri-implant diseases has greatly expanded. The clinical manifestations, in the absence of a globally established classification, are peri-implant mucositis and peri-implantitis, the counterparts of gingivitis and periodontitis, respectively. However, many doubts remain about their features. Official diagnostic criteria, globally recognised by the dental community, have not yet been introduced. The review presented possible association between gastrointestinal diseases and peri-implant diseases. Previous studies had revealed the association with significantly higher levels of bacteria in patient’s gastrointestinal disease at either gingivitis or in periodontitis site. Additionally, pathogenesis of the periodontitis is similar to peri-implant diseases.
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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Diseases":

1

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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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.
3

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.
4

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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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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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.
7

Gadd, Malin. "Cardiovascular diseases in immigrants in Sweden /." Stockholm : Neurotec, Center for family and community medicine, Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7140-627-1/.

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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
9

Rodeiro, Carmen Lucia Vidal. "Some issues in disease map modelling and surveillance of diseases." Thesis, University of Aberdeen, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415553.

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The first part of this thesis is dedicated to the study of edge effects in maps of disease.  The aim of the analyses is to find out how the estimation of the risk from a disease near boundaries can be affected by the boundary position.  The behaviour of a selection of models for disease mapping is evaluated when different edge conditions exist in the data. Disease mapping plays an important role in monitoring the health of a community.  Plotting new cases on a map is a frequently used technique for monitoring the spread of infectious diseases and from a statistical point of view it is relevant to consider how statistical methods can be developed or employed to aid the task of surveillance.  In the second part of this thesis, methodological and practical issues in developing a rapid response in a spatial surveillance system are discussed.  In particular, I review and propose methods for the detection of changes.  A simulation study is set up to assess if these methods are good at detecting changes in risk over space and time.  An application to a real data set is also given. Surveillance should be performed as quickly as possible but complex Bayesian models require the use of sampling methods to provide estimates of posterior expectations, and these estimates may be computationally expensive to obtain.  To aid this, special computational approaches can be considered.  One option is to resample the output form initial iterations to provide reweighted estimates as time protocols.  This is known a filtration or sequential Monte Carlo.  In the third part of this thesis I review the use of sequential Monte Carlo methods (in particular, the Resample-Move algorithm) for dynamic systems, focusing on their use in a surveillance context.  This is followed by an application to a real data set where a comparison between the use of McMC methods and the Resample-Move algorithm is carried out.
10

Schwengler, Franziska. "Prion Diseases." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-36790.

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Books on the topic "Diseases":

1

Surendran, Sankar. Neurochemistry of metabolic diseases: Lysosomal storage diseases, phenylketonuria, and Canavan disease. New York: Nova Science Publishers, 2012.

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

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Corporation, Springhouse, ed. Diseases. 3rd ed. Springhouse, Pa: Springhouse Corp., 2001.

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Corporation, Springhouse, ed. Diseases. Springhouse, Pa: Springhouse Corp., 1993.

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

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Werker, Paul M. N., Joseph Dias, Charles Eaton, Bert Reichert, and Wolfgang Wach, eds. Dupuytren Disease and Related Diseases - The Cutting Edge. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-32199-8.

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Churg, Jacob. Renal disease: Classification and atlas of glomerular diseases. 2nd ed. New York: Igaku-Shoin, 1995.

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Monette, P. L. Grape diseases: Corky bark disease and stem pitting. Toronto, Ont: Ministry of Agriculture and Food, 1993.

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Sheen, Barbara. Diseases and Disorders - Heart Disease (Diseases and Disorders). Lucent Books, 2004.

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Abramovitz, Melissa. Diseases and Disorders - Parkinson's Disease (Diseases and Disorders). Lucent Books, 2004.

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Book chapters on the topic "Diseases":

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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 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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Misra, Ashok K. "Diseases." In Guava: botany, production and uses, 285–328. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781789247022.0015.

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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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Conference papers on the topic "Diseases":

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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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Mesihović-Dinarević, Senka, Mirza Halimić, and Almira Kadić. "ACQUIRED AND GENETICALLY PREDISPOSED HEART DISEASE IN CHILDREN." In Acquired Heart Diseases. Academy of Sciences and Arts of Bosnia and Herzegovina, 2015. http://dx.doi.org/10.5644/pi2015-158-01.

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Omerčahić-Dizdarević, Aida, Velma Selmanović, and Adisa Čengić. "RHEUMATIC FEVER: A DISEASE THAT SHOULD NOT YET BE FORGOTTEN." In Acquired Heart Diseases. Academy of Sciences and Arts of Bosnia and Herzegovina, 2015. http://dx.doi.org/10.5644/pi2015-158-02.

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Begić, Fatima. "ACQUIRED VALVULAR HEART DISEASE IN CHILDREN: OUR EXAMPLES." In Acquired Heart Diseases. Academy of Sciences and Arts of Bosnia and Herzegovina, 2015. http://dx.doi.org/10.5644/pi2015-158-03.

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Cerić, Šejla, and Elma Kučukalić-Selimović. "THE IMPORTANCE OF PHARMACOLOGICAL STRESS IN MYOCARDIAL PERFUSION SCINTIGRAPHY." In Acquired Heart Diseases. Academy of Sciences and Arts of Bosnia and Herzegovina, 2015. http://dx.doi.org/10.5644/pi2015-158-04.

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Kušljugić, Zumreta, and Katarina Kovačević. "BRUCELLA ENDOCARDITIS: A CASE STUDY." In Acquired Heart Diseases. Academy of Sciences and Arts of Bosnia and Herzegovina, 2015. http://dx.doi.org/10.5644/pi2015-158-05.

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Kulić, Mehmed, Ibrahim Terzić, Mirza Dilić, Elnur Tahirović, and Muhamed Spužić. "PRIMARY PERCUTANEOUS CORONARY INTERVENTIONS NETWORK IN BOSNIA AND HERZEGOVINA." In Acquired Heart Diseases. Academy of Sciences and Arts of Bosnia and Herzegovina, 2015. http://dx.doi.org/10.5644/pi2015-158-06.

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Haxhibeqiri-Karabdić, Ilirijana, Emir Kabil, and Haris Vranić. "ISCHAEMIC HEART DISEASE – SURGICAL TREATMENT AND POST-OPERATIVE COMPLICATIONS." In Acquired Heart Diseases. Academy of Sciences and Arts of Bosnia and Herzegovina, 2015. http://dx.doi.org/10.5644/pi2015-158-07.

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Pandur, Sanko. "REVIEW UP-TO-DATE CORONARY ARTERY BYPASS GRAFT SURGERY." In Acquired Heart Diseases. Academy of Sciences and Arts of Bosnia and Herzegovina, 2015. http://dx.doi.org/10.5644/pi2015-158-08.

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Reports on the topic "Diseases":

1

Ogden, N. H., C. Bouchard, G. Brankston, E. M. Brown, T. Corrin, A. Dibernardo, M A Drebot, et al. Infectious diseases. Natural Resources Canada/CMSS/Information Management, 2022. http://dx.doi.org/10.4095/329532.

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2

Vlasova, Liubov, Olesya Musina, Lidia Timeeva, and Irina Yarunina. Occupational Diseases. SIB-Expertise, July 2022. http://dx.doi.org/10.12731/er0597.29072022.

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Abstract:
Авторы данного электронного образовательного ресурса разработали систему упражнений, нацеленных на овладение студентами профессиональной медицинской лексикой и формирование навыков работы с аутентичными текстами по тематике «Профессиональные заболевания». Данный образовательный ресурс включает в себя пять модулей, описывающих виды и симптомы профессиональных заболеваний. Каждый модуль содержит аутентичные тексты, позволяющие студентам ознакомиться с вышеуказанной тематикой на английском языке. Отличительной чертой данного ЭОРа является то, что после каждого текста представлен ряд лексико-грамматических упражнений на формирование навыков работы с медицинской лексикой, а также ряд упражнений, направленных на формирование навыков работы с содержанием текста и пониманием ключевой информации. Глоссарий в конце данного образовательного ресурса содержит все ключевые слова и выражения, представленные в каждом модуле. Структура электронного образовательного ресурса позволяет в полной мере выполнять задачи овладения медицинской профессиональной лексикой и навыками устной речи. Данный электронный ресурс позволяет студентам заниматься как в аудитории, так и самостоятельно.
3

Wise, Kiersten, Carl Bradley, Loren Giesler, Bill Johnson, Travis Legleiter, Mark Licht, Daren Mueller, et al. Soybean Seedling Diseases. United States: Crop Protection Netework, June 2015. http://dx.doi.org/10.31274/cpn-20190620-023.

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Lyons, Suzannah. Targeting infectious diseases. Monash University, February 2024. http://dx.doi.org/10.54377/7615-dbfa.

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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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Barros-Poblete, Marisol, Rodrigo Torres-Castro, Mauricio Henríquez, Anita Guequen, Isabel Blanco, and Carlos Flores. Dysbiosis as a prognostic factor for clinical worsening in chronic respiratory disease: A systematic review and metanalysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0089.

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Abstract:
Review question / Objective: Is dysbiosis a prognostic factor for clinical worsening in patients with chronic respiratory diseases?. Condition being studied: Dysbiosis, defined as changes in the quantitative and qualitative composition of the microbiota. Eligibility criteria: Over 18 years old adult patients with chronic respiratory diseases clinical diagnosis (cystic fibrosis, chronic obstructive pulmonary disease, asthma, idiopathic pulmonary fibrosis, interstitial lung disease, sarcoidosis, bronchiectasis, non-CF bronchiectasis, pulmonary hypertension) according to the International Statistical Classification of Diseases and Related Health Problems (ICD) from OMS) and international guidelines of each disease.
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Freeman, Stanley, and Daniel Legard. Epidemiology and Etiology of Colletotrichum Species Causing Strawberry Diseases. United States Department of Agriculture, September 2001. http://dx.doi.org/10.32747/2001.7695845.bard.

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Abstract:
Diseases caused by Colletotrichum spp. are one of the most important limitations on international strawberry production, affecting all vegetative and fruiting parts of the plant. From 1995 to 1997, C. acutatum infections reached epidemic levels in Israeli strawberry nurseries, causing extensive loss of transplants in fruit-bearing fields and additional reductions in yield. Although C. acutatum also occurs on strawberry in Florida, recent crown rot epidemics have been primarily caused by C. gloeosporioides. Little is known about the basic epidemiology of these important diseases on strawberry. The source of initial inoculum for epidemics in Israel, Florida (other US states including California) and the rest of the world is not well understood. Subspecies relationships between Colletotrichum isolates that cause the different diseases on strawberry (i.e. attack different tissues) are also not well understood. Objectives of this proposal were to detennine the potential of infested soil, strawberry debris and other hosts as sources of primary inoculum for strawberry diseases caused by Colletotrichum spp. in Israel and Florida. In addition, traditional (ie. morphological characteristics, benomyl sensitivity, vegetative compatibility grouping) and DNA based methods were used to investigate the etiology of these diseases in order to resolve epidemiologically important subspecies variation. In Israel it was found that C. gloeosporioides and C. acutatum infecting strawberry could remain viable in sterilized soil for up to one year and in methyl-bromide fumigated soil for up to 4 months; inoculum in mummified fruit remained viable for at least 5 months under field conditions whereas that in infected crowns was not recovered. Therefore, the contribution of these inocula to disease epidemics should be considered. The host range and specificity of C. acutatum from strawberry was examined on pepper, eggplant, tomato, bean and strawberry under greenhouse conditions. The fungus was recovered from all plant species over a three-month period but caused disease symptoms only on strawberry. C. acutatum was also isolated from healthy looking, asymptomatic plants of the weed species, Vicia and Conyza, growing in infected strawberry fruiting fields. Isolates of C. acutatum originating from strawberry and anemone infected both plant species in artificial inoculations. The habitation of a large number of plant species including weeds by C. acutatum suggests that although it causes disease only on strawberry and anemone in Israel, these plants may serve as a potential inoculum source for strawberry infection and pennit survival of the pathogen between seasons. In Florida, isolates of Colletotrichum spp. from diseased strawberry fruit and crowns were evaluated to detennine their etiology and the genetic diversity of the pathogens. Only C. acutatum was recovered from fruit and C. gloeosporioides were the main species recovered from crowns. These isolates were evaluated at 40 putative genetic loci using random amplified polymorphic DNA (RAPD). Genetic analysis of RAPD markers revealed that the level of linkage disequilibrium among polymorphic loci in C. gloeosporioides suggested that they were a sexually reproducing population. Under field conditions in Florida, it was detennined that C. gloeosporioides in buried crowns survived
8

Westergaard, Jørgen M. Wildlife and Infectious Animal Diseases. Nordic Council of Ministers, March 2014. http://dx.doi.org/10.6027/tn2014-508.

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M. Westergaard, Jørgen. Contingency Planning for Animal Diseases. Nordic Council of Ministers, March 2014. http://dx.doi.org/10.6027/tn2014-509.

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10

Tignor, Gregory H. Drug Development against Viral Diseases. Fort Belvoir, VA: Defense Technical Information Center, February 1987. http://dx.doi.org/10.21236/ada201949.

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