Relevant bibliographies by topics / Mechanisms of disease

Contents

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

Academic literature on the topic 'Mechanisms of disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Mechanisms of disease"

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Samson, Kurt. "Disease Mechanisms-Alzheimerʼs Disease." Neurology Today 18, no. 14 (July 2018): 1. http://dx.doi.org/10.1097/01.nt.0000544100.70517.f7.

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Talan, Jamie. "Disease Mechanisms-Neurodegenerative Disease." Neurology Today 18, no. 16 (August 2018): 1. http://dx.doi.org/10.1097/01.nt.0000544621.18582.bc.

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Talan, Jamie. "Disease Mechanisms-Neurodegenerative Disease." Neurology Today 18, no. 19 (October 2018): 51–53. http://dx.doi.org/10.1097/01.nt.0000547371.17110.51.

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Talan, Jamie. "Disease Mechanisms-Pickʼs Disease." Neurology Today 18, no. 20 (October 2018): 7–8. http://dx.doi.org/10.1097/01.nt.0000547506.22698.88.

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Talan, Jamie. "Disease Mechanisms-Parkinsonʼs Disease." Neurology Today 18, no. 21 (November 2018): 1. http://dx.doi.org/10.1097/01.nt.0000547814.01174.f5.

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Ramos, Guilherme Piovezani, and Konstantinos A. Papadakis. "Mechanisms of Disease: Inflammatory Bowel Diseases." Mayo Clinic Proceedings 94, no. 1 (January 2019): 155–65. http://dx.doi.org/10.1016/j.mayocp.2018.09.013.

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Barbour, Virginia, and Richard Horton. "Mechanisms of disease." Lancet 359, no. 9300 (January 2002): 2–3. http://dx.doi.org/10.1016/s0140-6736(02)07268-9.

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Collins, Thomas R. "Disease Mechanisms-Migraine." Neurology Today 18, no. 12 (June 2018): 23–24. http://dx.doi.org/10.1097/01.nt.0000541353.78697.66.

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Seufferlein, T. "Mechanisms of Disease." Zeitschrift für Gastroenterologie 43, no. 10 (October 12, 2005): 1111. http://dx.doi.org/10.1055/s-2005-858669.

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Hurley, Dan. "Disease Mechanisms-Epilepsy." Neurology Today 18, no. 14 (July 2018): 1. http://dx.doi.org/10.1097/01.nt.0000544102.64679.79.

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Dissertations / Theses on the topic "Mechanisms of disease"

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Miller, Aaron. "Black Band Disease: Elucidating Origins and Disease Mechanisms." FIU Digital Commons, 2012. http://digitalcommons.fiu.edu/etd/558.

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Coral diseases were unknown in the scientific community fifty years ago. Since the discovery of a coral disease in 1965, there has been an exponential increase in the number of known coral diseases, as the abundance, prevalence, distribution, and number of host species affected has also significantly increased. Coral diseases are recognized as contributing significantly to the dramatic losses of coral cover on a global basis, particularly in the Caribbean. The apparent sudden emergence of coral diseases suggests that they may be a symptom of an overall trend associated with changing environmental conditions. However, not much evidence has been gathered to address this question. The following studies were designed to build a comprehensive argument to support this hypothesis for one important coral disease – black band disease (BBD). A meta-analysis of clone libraries identifying the microbial communities associated with BBD reveal important information including that a single cyanobacterial operational taxonomic unit (OTU) was by far the most prevalent OTU in diseased samples, and that the alphaproteobacteria, which include some of the most common bacteria in marine waters, were the most diversely represented. The analysis also showed that samples exhibited regional similarities. An fine and ultrastructural characterization of the disease revealed that the cyanobacteria are prolific borers through the coral skeleton, and that the cyanobacteria penetrate coral tissue, leading to their presence ahead of the main migrating disease band. It was further found that apparently healthy corals exposed to toxins found in BBD, exhibited similar tissue degradation to those infected with BBD. Comparing the disease progression to biofilm formation, it was determined that scouting cyanobacteria may contribute to the migration of the disease through progressive biofilm development over intact coral tissue. Together, these studies provide significant evidence for the hypothesis that BBD is an opportunistic disease, caused by common environmental bacteria, facilitated by the changing environmental conditions associated with climate change.
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Palmer, Samantha Jane. "Compensatory mechanisms in Parkinson's disease." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/22661.

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Parkinson’s disease (PD) is a common movement disorder, affecting 1% of the population over the age of 65. Pathologically, PD results from degeneration of nigral dopaminergic neurons, however symptoms do not appear until an estimated 50% of these cells are lost, suggesting compensatory mechanisms exist which mask disease onset, and may later delay progression of the disease. Compensation may take place over various spatial and temporal scales, from changes in synaptic dopamine release and synthesis that take place over a period of minutes, to recruitment of novel, widespread networks of brain regions for a specific task, which may require formation of new connections over an extended period of time. Neuroimaging techniques have recently allowed the investigation of regional and network changes in activation related to motor performance in PD, however the question of whether such changes represent a downstream effect of basal ganglia degeneration, or a compensatory change, remains difficult to determine. Here, we applied an approach from research into Alzheimer’s Disease, where abnormal activation patterns are studied in the context of tasks of increasing difficulty, such that inferences regarding their compensatory nature can be made. We show that individuals with PD are able to increase the recruitment of normal networks for a motor task (motor reserve) as a form of compensation, in addition to compensatory recruitment of novel networks to accomplish the same task as healthy controls. In particular, we observe a switch from striato-thalamo-cortical (STC) motor loops to cerebello-thalamo-cortical (CTC) loops as a compensatory strategy. This compensatory recruitment involves changes in the amplitude, spatial extent, and connectivity of regions within the CTC pathway. However, this compensation does not come without a price, since we show that compensatory CTC recruitment involving disconnection between the STC and CTC loops occurs in subjects with tremor-dominant PD, but not akinetic-rigidity-dominant PD, supporting a growing body of evidence that suggests the cerebellum plays an important role in the generation of PD tremor. Together, this body of research has implications for treatments that target the symptom of tremor in PD, as therapies which minimize tremor might also reduce beneficial aspects of compensation.
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Bourne, Nathan T. "Molecular mechanisms of Alzheimer's disease." Thesis, University of Sheffield, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521906.

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Freeburn, Jennifer. "Haemostatic mechanisms in vascular disease." Thesis, University of Ulster, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390118.

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Zhang, Li. "Immunological mechanisms in autoimmune disease." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308276.

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Freese, Andrew. "Excitotoxic mechanisms in Huntington's disease." Thesis, Massachusetts Institute of Technology, 1991. http://hdl.handle.net/1721.1/17295.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Whitaker College of Health Sciences and Technology, 1992.
Includes bibliographical references (leaves 191-250).
by Andrew Freese.
Ph.D.
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Vadnal, Jonathan. "Epigenetic Mechanisms in Neurodegenerative Disease." Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1353955013.

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Harcombe, Alun Andrew. "Immunological mechanisms in cardiac disease." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/20552.

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The aim of the work presented in this thesis was to examine cell and antibody-mediated immune mechanisms in heart muscle disease. The two conditions studied were acute rejection of cardiac allografts as an example of cell-mediated immune damage, and alcoholic heart muscle disease as a potential example of antibody-mediated disease. In the first study, experiments were performed on 94 endomyocardial biopsies (EMB) from 73 patients to determine the relationship between the ability to grow lymphocytes from EMB in culture and (i) grade of concurrent or future rejections, (ii) the presence of endocardial lymphocytic infiltrates (ELI), and (iii) donor/recipients HLA mismatches. These studies showed that outgrowth of lymphocytes was not closely related to the degree of rejection, not influenced by the use of polyclonal activators in the medium but it was affected by the presence to two HLA mismatches at the DR locus. The presence of ELI was related to rejection but not to outgrowth of the lymphocytes. It was concluded that, contrary to predictions in the literature, the ability to grow lymphocytes from EMB did not indicate presence of impending injection. In the second study, experiments were performed to test the hypothesis that alcoholic heart muscle disease may be caused by autoantibodies to acetaldehyde-modified myocardial proteins. Sera from 61 subjects were tested by Western analysis for antibodies against acetaldehyde-treated human myocardial proteins. No such antibodies were detected in 11 healthy controls subjects, or 28 patients with non-alcoholic heart diseases. In contrast, 4 out of 14 patients with alcoholic heart disease (28%) had detectable antibodies, suggesting a role for these antibodies in alcohol-induced heart muscle disease. To isolate potential antigenic myocardial proteins from small samples of myocardium a technique was developed for rapidly electroeluting proteins separated on a polyacrylamide gel. This system was validated by electroeluting endothelin receptors from human myocardium.
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O'Regan, David. "Mechanisms of glucocorticoid programmed disease." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/27148.

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This thesis investigates the role of the renin-angiotensin (RAS), and sympathetic nervous systems (SNS) in determining programmed hypertension, and further seeks to determine whether programming effects are sexually dimorphic. DEX administration in the last week of gestation reduces offspring birth weight and programmes adult cardiovascular and metabolic physiology in a sex specific manner. In male offspring, prenatal glucocorticoid exposure programmes elevated basal circulating corticosterone, elevated PEPCK activity, and produces adulthood postglucose hyperglycaemia and hyperinsulinaemia. Whilst in female offspring, prenatal DEX programmes elevated hepatic angiotensinogen mRNA expression, elevated plasma angiotensinogen and renin activity, and produces hypertension, when measured by tail-cuff plethysmography. Unlike previous studies, offspring blood pressure was subsequently assessed with radiotelemetry, which is unmarred by any stress artefact. We no demonstrate that prenatal DEX-treated male and female offspring actually display lower basal blood pressure in adulthood; with the commonly expected hypertensive phenotype only being noted when these offspring are subjected to any stressor. Moreover, DEX-treated offspring sustain their stress-induced hypertension for longer. These hypertensive responses are mediated by alterations in the responsitivity of the sympathetic nervous system, being ameliorated by the inhibition of catecholamine synthesis, and further exaggerated by the promotion of systemic catecholamine release. Additionally, we demonstrate that DEX-treated offspring display greater sensitivity to various vasoconstrictors in the isolated mesenteric vasculature. These findings demonstrate that in utero over-exposure to glucocorticoids actually results in stress-induced hypertension, and support a role for both RAS and SNS in mediating this. Furthermore, it appears that the programming of cardiovascular physiology may reflect distinct processes in each gender, whilst the programming of metabolic physiology is male specific.
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James, V. M. "Molecular insights into the disease mechanisms of startle disease." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1379645/.

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This study describes an in-depth investigation into the pathogenic mechanisms of inherited mutations that lead to disorders of inhibitory glycinergic transmission, primarily the rare human disorder known as startle disease/hyperekplexia. I also investigated mutations causing a similar startle phenotype in cows, mice and zebrafish. Using molecular genetics techniques, I identified pathogenic mutations in the genes that encode for proteins involved in glycinergic neurotransmission, specifically the postsynaptic glycine receptor (GlyR) subunits and the presynaptic glycine transporter GlyT2. Using homology modelling and other computational biology methods, I examined the structural and functional impacts of mutations on protein function, revealing key motifs and amino acids crucial for receptor and transporter activity. Using cDNA cloning and site-directed mutagenesis, I also generated expression constructs for wild-type and mutant proteins that were used in functional tests to measure the impact of pathogenic mutations on glycine receptor and transporter function. For certain animal models of startle disease, I was also able to develop diagnostic PCR tests for pathogenic mutations, which can be used to alleviate further animal suffering by preventing ‘at risk matings’ of carrier animals. Taken together, my findings reveal several new pathogenic mechanisms of GlyR and GlyT2 mutations in startle disease in humans and animals, revealing insights into receptor and transporter function that may be applicable to other neurological disorders.
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Books on the topic "Mechanisms of disease"

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Blass, John P. Neurochemical mechanisms in disease. New York: Springer, 2011.

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Fitridge, Robert, ed. Mechanisms of Vascular Disease. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43683-4.

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Blass, John P., ed. Neurochemical Mechanisms in Disease. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-7104-3.

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Freeburn, Jennifer. Haemostatic mechanisms in vascular disease. [S.l: The Author], 1996.

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Engleberg, N. Cary, Moselio Schaechter, Victor J. DiRita, and Terence Dermody. Schaechter's mechanisms of microbial disease. 5th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2013.

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Ocular disease: Mechanisms and management. [Philadelphia]: Saunders/Elsevier, 2010.

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Molinoff, Perry B. Peptic ulcer disease: Mechanisms & management. Rutherford, NJ: Healthpress Publishing Group, Inc., 1990.

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Schaechter's mechanisms of microbial disease. 5th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2013.

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Guadalupe, Garcia-Tsao, and SpringerLink (Online service), eds. Vascular Liver Disease: Mechanisms and Management. New York, NY: Springer Science+Business Media, LLC, 2011.

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Human physiology and mechanisms of disease. 5th ed. Philadelphia: W.B. Saunders, 1992.

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Book chapters on the topic "Mechanisms of disease"

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Direskeneli, Haner, and Güher Saruhan-Direskeneli. "Disease Mechanisms." In Behçet’s Syndrome, 243–64. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-5641-5_14.

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Direskeneli, Haner, and Güher Saruhan-Direskeneli. "Disease Mechanisms." In Behçet Syndrome, 209–22. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24131-5_15.

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Laugier, R. "Cellular Secretory Mechanisms." In Pancreatic Disease, 153–60. London: Springer London, 1991. http://dx.doi.org/10.1007/978-1-4471-3356-8_13.

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Hanck, Ch, and M. V. Singer. "Mechanisms in Cellular Injury." In Pancreatic Disease, 36–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60068-5_4.

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Suzuki, Jiro. "Mechanisms of Symptomatic Occurrence." In Moyamoya Disease, 53–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-95483-2_4.

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Vonsattel, Jean Paul G., Giuliano Binetti, and Lynne M. Kelley. "Pick Disease." In Molecular Mechanisms of Dementia, 253–69. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-59259-471-9_16.

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Schölmerich, J. "Immunological Mechanisms in Acute Pancreatitis." In Pancreatic Disease, 24–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60068-5_3.

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Blass, John P. "Mechanisms Versus Diagnoses." In Neurochemical Mechanisms in Disease, 1–15. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7104-3_1.

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Peakman, M., D. Vergani, and A. L. W. F. Eddleston. "Mechanisms of Autoimmunity." In Immunology of Liver Disease, 85–109. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1428-8_6.

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Quyyumi, A. A. "Mechanisms of angina pectoris." In Ischaemic Heart Disease, 91–121. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3211-1_4.

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Conference papers on the topic "Mechanisms of disease"

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Gautieri, Alfonso, Sebastien Uzel, Simone Vesentini, Alberto Redaelli, and Markus J. Buehler. "Osteogenesis Imperfecta: Molecular and Mesoscale Disease Mechanisms." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204530.

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Osteogenesis Imperfecta (OI) is a genetic disorder in collagen characterized by mechanically weakened tendon and fragile bones that affects more than 1 in 10,000 individuals. Even though many studies have attempted to associate specific mutation types with phenotypic severity, the mechanisms by which a single point mutation influences the mechanical behavior of tissues at multiple length-scales remain unknown. Here we show by a hierarchy of full atomistic and mesoscale simulation that OI mutations severely compromise the mechanical properties of collagenous tissues at multiple scales, from single molecules to collagen fibrils.
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Sharan, Roded. "Invited: From protein networks to disease mechanisms." In 2012 IEEE 2nd International Conference on Computational Advances in Bio and Medical Sciences (ICCABS). IEEE, 2012. http://dx.doi.org/10.1109/iccabs.2012.6182624.

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Yogev, Or, Andrew A. Shapiro, and Erik K. Antonsson. "Growth control and disease mechanisms in computational embryogeny." In the 10th annual conference. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1389095.1389265.

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Uzel, Sebastien, and Markus J. Buehler. "Molecular and Mesoscale Mechanisms of Osteogenesis Imperfecta Disease." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13160.

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Collagen is a crucial structural protein material, formed through a hierarchical assembly of tropocollagen molecules, arranged in collagen fibrils that constitute the basis for larger-scale fibrils and fibers. Osteogenesis imperfecta is a genetic disorder in collagen characterized by mechanically weakened tendon, fragile bones, skeletal deformities and in severe cases prenatal death. Even though many studies have attempted to associate specific mutation types with phenotypic severity, the mechanisms by which a single point mutation influences the mechanical behavior of tissues at multiple length-scales remain unknown. In this study, we report a series of systematic molecular scale based bottom-up computational experiments focused on pure collagenous tissue, carried out using atomistic-level molecular dynamics (MD), adaptive Poison-Boltzmann solver (APBS) calculations, and a mesoscale molecular model of collagen fibrils.
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Frankenberg Garcia, J., C. Michaeloudes, B. Xu, K. F. Chung, S. E. Harding, T. A. Rodriguez, and P. K. Bhavsar. "Mechanisms of Mitochondrial Transfer in Health and Disease." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7217.

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Halasa, Salaheldin, Praveen Arany, and Michael R. Hamblin. "Nitromedicine: translating alternative medicine to evidence based medicine and redefining disease (Conference Presentation)." In Mechanisms of Photobiomodulation Therapy XI, edited by Michael R. Hamblin, James D. Carroll, and Praveen Arany. SPIE, 2016. http://dx.doi.org/10.1117/12.2226027.

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Ferdous, Zannatul, Hanjoong Jo, and Robert M. Nerem. "Differential Osteogenic Marker Expression by Human Vascular and Valvular Cells in Tissue-Engineered Collagen Constructs." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19424.

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Atherosclerosis and aortic stenosis are two of the most prevalent cardiovascular disorders and a major cause of death in elderly population. In atherosclerosis, plaques and calcium deposits build up inside major arteries, which lead to narrowing of the vessel lumens and limits or completely blocks blood flow. Similarly, in calcific aortic stenosis, calcium deposits on valve cusps and valve ring result in narrowing of valve lumen, eventually leading to impaired function and even valve failure. As the disease progresses, both diseases thus require expensive replacement/repair surgeries in most patients. However, in spite of the high prevalence, the causes and mechanisms of these diseases are still not clearly understood. Due to the similarities in diseased tissue pathology, atherosclerosis and aortic stenosis have been suggested to be continuum of the same disease [1] and mainly have been investigated for atherosclerosis. However, the prevalence of both diseases is not concurrent in most patients. Likewise, valvular interstitial cells (VICs) were thought to behave in a similar manner as smooth muscle cells (SMCs), but some recent studies suggest differences between the two cell types [2]. Therefore, unique mechanisms might be involved in how VICs and SMCs respond to an osteogenic environment.
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Larssen, Marte Strømsnes, Christian Hodnesdal, Ingunn Skjorten, Janne Mykland Hilde, Kjetil Steine, Knut Liestol, and Knut Gjesdal. "Mechanisms of ECG changes in chronic obstructive pulmonary disease." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2434.

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Carstensen, Marcus S., Martin Thorning-Schmidt, Mikkel Agger, N. Mai Nguyen, Jes Broeng, Troels W. Kjær, and Paul Michael Petersen. "Wavelength dependency of the critical flicker-fusion frequency: therapeutic 40 Hz light source in Alzheimer’s disease." In Mechanisms of Photobiomodulation Therapy XVI, edited by James D. Carroll, Praveen Arany, and Ann Liebert. SPIE, 2021. http://dx.doi.org/10.1117/12.2582940.

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Lin, Xiaotong, and Tingting Yan. "ALZHEIMER'S DISEASE: MECHANISMS OF TAU AND AMYLOID BETA-INDUCED EXCITOTOXICITY." In 2016 International Conference on Biotechnology and Medical Science. WORLD SCIENTIFIC, 2016. http://dx.doi.org/10.1142/9789813145870_0055.

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Reports on the topic "Mechanisms of disease"

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Miller, Sheldon S. Fluid Transport Mechanisms in Breast Gross Cystic Disease. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada382765.

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Sjogren, Maria H., and Brooke Huntley. Hepatitis C. Virus Infection: Mechanisms of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada477987.

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Grekhoff, R. A., V. L. Kedrova, G. P. Suleimanova, E. G. Korenskaya, and A. V. Aleksandrov. STUDY OF MECHANISMS OF PSYCHOLOGICAL DEFENSES IN PATIENTS WITH SYSTEMIC SCLEROSIS DEPENDING ON ACTIVITY OF THE DISEASE AND OTHER INDICES. "PLANET", 2019. http://dx.doi.org/10.18411/978-5-907192-54-6-2019-xxxvi-90-97.

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Shkolnikova, Maria A., Svetlana A. Shalnova, Vladimir M. Shkolnikov, Victoria A. Metelskaya, Alexander D. Deev, Evgueni M. Andreev, Dmitri A. Jdanov, and James W. Vaupel. Biological mechanisms of disease and death in Moscow: rationale and design of the survey on Stress Aging and Health in Russia (SAHR). Rostock: Max Planck Institute for Demographic Research, June 2009. http://dx.doi.org/10.4054/mpidr-wp-2009-016.

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Sjogren, Maria H., and Kent Holtzmuller. Hepatitis C Virus Infection: Mechanism of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada406083.

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Sjogren, Maria H. Hepatitis C. Virus Infection: Mechanism of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada433067.

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Cox, Daniel L., and Rajiv R. Singh. Theoretical Modeling of Molecular Mechanisms, Time Scales, and Strains in Prion Diseases. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada462946.

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Ibáñez, Ana María, Sandra Rozo, and Maria J. Urbina. Forced Migration and the Spread of Infectious Diseases. Inter-American Development Bank, November 2020. http://dx.doi.org/10.18235/0002894.

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We examine the role of Venezuelan forced migration on the propagation of 15 infectious dis-eases in Colombia. For this purpose, we use rich municipal-monthly panel data. We exploit the fact that municipalities closer to the main migration entry points have a disproportionate ex-posure to infected migrants when the cumulative migration flows increase. We find that higher refugee inflows are associated with increments in the incidence of vaccine-preventable dis-eases, such as chickenpox and tuberculosis, as well as sexually transmitted diseases, including AIDS and syphilis. However, we find no significant effects of migration on the propagation of vector-borne diseases. Contact with infected migrants upon arrival seems to be the main driving mechanism.
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Yang, Xinwei, Huan Tu, and Xiali Xue. The improvement of the Lower Limb exoskeletons on the gait of patients with spinal cord injury: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0095.

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Review question / Objective: The purpose of this systematic review and meta-analysis was to determine the efficacy of lower extremity exoskeletons in improving gait function in patients with spinal cord injury, compared with placebo or other treatments. Condition being studied: Spinal Cord Injury (SCI) is a severely disabling disease. In the process of SCI rehabilitation treatment, improving patients' walking ability, improving their self-care ability, and enhancing patients' self-esteem is an important aspect of their return to society, which can also reduce the cost of patients, so the rehabilitation of lower limbs is very important. The lower extremity exoskeleton robot is a bionic robot designed according to the principles of robotics, mechanism, bionics, control theory, communication technology, and information processing technology, which can be worn on the lower extremity of the human body and complete specific tasks under the user's control. The purpose of this study was to evaluate the effect of the lower extremity exoskeleton on the improvement of gait function in patients with spinal cord injury.
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10

Matthew, Gray. Data from "Winter is Coming – Temperature Affects Immune Defenses and Susceptibility to Batrachochytrium salamandrivorans". University of Tennessee, Knoxville Libraries, January 2021. http://dx.doi.org/10.7290/t7sallfxxe.

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Environmental temperature is a key factor driving various biological processes, including immune defenses and host-pathogen interactions. Here, we evaluated the effects of environmental temperature on the pathogenicity of the emerging fungus, Batrachochytrium salamandrivorans (Bsal), using controlled laboratory experiments, and measured components of host immune defense to identify regulating mechanisms. We found that adult and juvenile Notophthalmus viridescens died faster due to Bsal chytridiomycosis at 14 ºC than at 6 and 22 ºC. Pathogen replication rates, total available proteins on the skin, and microbiome composition likely drove these relationships. Temperature-dependent skin microbiome composition in our laboratory experiments matched seasonal trends in wild N. viridescens, adding validity to these results. We also found that hydrophobic peptide production after two months post-exposure to Bsal was reduced in infected animals compared to controls, perhaps due to peptide release earlier in infection or impaired granular gland function in diseased animals. Using our temperature-dependent infection results, we performed a geographic analysis that suggested that N. viridescens populations in the northeastern United States and southeastern Canada are at greatest risk for Bsal invasion. Our results indicate that environmental temperature will play a key role in the epidemiology of Bsal and provide evidence that temperature manipulations may be a viable Bsal management strategy.
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