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Journal articles on the topic 'Disease propagation'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Nagaprasad, S., T. Pushpalatha, and S. Naga Lakshmi. "Heart Disease Prediction Propagation approach." International Journal of Machine Learning and Networked Collaborative Engineering 4, no. 2 (October 24, 2020): 72–77. http://dx.doi.org/10.30991/ijmlnce.2020v04i02.003.

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2

Brightman, B. K., Q. X. Li, D. J. Trepp, and H. Fan. "Differential disease restriction of Moloney and Friend murine leukemia viruses by the mouse Rmcf gene is governed by the viral long terminal repeat." Journal of Experimental Medicine 174, no. 2 (August 1, 1991): 389–96. http://dx.doi.org/10.1084/jem.174.2.389.

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Neonatal CxD2 (Rmcfr) and Balb/c (Rmcfs) mice inoculated with Moloney murine leukemia virus (M-MuLV) exhibited approximately equivalent time course and pathology for disease. CxD2 mice showed only slightly reduced presence of Moloney mink cell focus-forming virus (M-MCF) provirus as seen by Southern blot analysis compared to Balb/c mice. This lack of restriction for disease and spread of MCF was in sharp contrast to that seen for CxD2 mice inoculated with Friend murine leukemia virus (F-MuLV), where incidence of disease and propagation of MCFs were severely restricted, as previously reported. Inoculation of CxD2 mice with FM-MuLV, a recombinant F-MuLV virus containing M-MuLV LTR sequences (U3 and R), resulted in T cell disease of time course equal to that seen in Balb/c mice; there also was little restriction for propagation of MCFs. This indicated that presence of the M-MuLV long terminal repeat (LTR) was sufficient for propagation of MCFs in CxD2 mice. Differing restriction for F-MuLV vs. M-MuLV in CxD2 mice was explained on the basis of different "MCF propagator cells" for the two viruses. It was suggested that cells propagating F-MCF (e.g., erythroid progenitors) are blocked by endogenous MCF-like gp70env protein, whereas cells propagating M-MCF (e.g., lymphoid) do not express this protein on their surface. F-MuLV disease in CxD2 mice was greatly accelerated when neonates were inoculated with a F-MuLV/F-MCF pseudotypic mixture. However, F-MCF provirus was not detectable or only barely detectable in F-MuLV/F-MCF-induced tumors, suggesting that F-MCF acted indirectly in induction of these tumors.

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3

Rajna, Zalán, Heli Mattila, Niko Huotari, Timo Tuovinen, Johanna Krüger, Sebastian C. Holst, Vesa Korhonen, et al. "Cardiovascular brain impulses in Alzheimer’s disease." Brain 144, no. 7 (March 31, 2021): 2214–26. http://dx.doi.org/10.1093/brain/awab144.

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Abstract Accumulation of amyloid-β is a key neuropathological feature in brain of Alzheimer’s disease patients. Alterations in cerebral haemodynamics, such as arterial impulse propagation driving the (peri)vascular CSF flux, predict future Alzheimer’s disease progression. We now present a non-invasive method to quantify the three-dimensional propagation of cardiovascular impulses in human brain using ultrafast 10 Hz magnetic resonance encephalography. This technique revealed spatio-temporal abnormalities in impulse propagation in Alzheimer’s disease. The arrival latency and propagation speed both differed in patients with Alzheimer’s disease. Our mapping of arterial territories revealed Alzheimer’s disease-specific modifications, including reversed impulse propagation around the hippocampi and in parietal cortical areas. The findings imply that pervasive abnormality in (peri)vascular CSF impulse propagation compromises vascular impulse propagation and subsequently glymphatic brain clearance of amyloid-β in Alzheimer’s disease.

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4

Wilson, Spencer, Abdullah Alabdulkarim, and David Goldsman. "Green Simulation of Pandemic Disease Propagation." Symmetry 11, no. 4 (April 22, 2019): 580. http://dx.doi.org/10.3390/sym11040580.

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This paper is concerned with the efficient stochastic simulation of multiple scenarios of an infectious disease as it propagates through a population. In particular, we propose a simple “green” method to speed up the simulation of disease transmission as we vary the probability of infection of the disease from scenario to scenario. After running a baseline scenario, we incrementally increase the probability of infection, and use the common random numbers variance reduction technique to avoid re-simulating certain events in the new scenario that would not otherwise have changed from the previous scenario. A set of Monte Carlo experiments illustrates the effectiveness of the procedure. We also propose various extensions of the method, including its use to estimate the sensitivity of propagation characteristics in response to small changes in the infection probability.

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5

Yates, Darran. "Propagation of disease pathology in PD." Nature Reviews Neurology 5, no. 10 (October 2009): 522. http://dx.doi.org/10.1038/nrneurol.2009.142.

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6

MAGDOŃ-MAKSYMOWICZ, M. S., A. Z. MAKSYMOWICZ, and J. GOŁDASZ. "SIMULATION OF MAD COW DISEASE PROPAGATION." International Journal of Modern Physics C 17, no. 02 (February 2006): 213–22. http://dx.doi.org/10.1142/s0129183106008935.

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Computer simulation of dynamic of BSE disease is presented. Both vertical (to baby) and horizontal (to neighbor) mechanisms of the disease spread are considered. The game takes place on a two-dimensional square lattice Nx×Ny = 1000×1000 with initial population randomly distributed on the net. The disease may be introduced either with the initial population or by a spontaneous development of BSE in an item, at a small frequency. Main results show a critical probability of the BSE transmission above which the disease is present in the population. This value is vulnerable to possible spatial clustering of the population and it also depends on the mechanism responsible for the disease onset, evolution and propagation. A threshold birth rate below which the population is extinct is seen. Above this threshold the population is disease free at equilibrium until another birth rate value is reached when the disease is present in population. For typical model parameters used for the simulation, which may correspond to the mad cow disease, we are close to the BSE-free case.

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7

Soto, Claudio, and Gabriela P. Saborı́o. "Prions: disease propagation and disease therapy by conformational transmission." Trends in Molecular Medicine 7, no. 3 (March 2001): 109–14. http://dx.doi.org/10.1016/s1471-4914(01)01931-1.

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8

Luk, Kelvin C., and Virginia M. Y. Lee. "Modeling Lewy pathology propagation in Parkinson's disease." Parkinsonism & Related Disorders 20 (January 2014): S85—S87. http://dx.doi.org/10.1016/s1353-8020(13)70022-1.

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9

Potterat, J. J., R. B. Rothenberg, and S. Q. Muth. "Network structural dynamics and infectious disease propagation." International Journal of STD & AIDS 10, no. 3 (March 1999): 182–85. http://dx.doi.org/10.1258/0956462991913853.

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10

Qian, Yu, Søren Besenbacher, Thomas Mailund, and Mikkel Heide Schierup. "Identifying disease associated genes by network propagation." BMC Systems Biology 8, Suppl 1 (2014): S6. http://dx.doi.org/10.1186/1752-0509-8-s1-s6.

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11

Wang, Yubo, Gaoxi Xiao, Limsoon Wong, Xiuju Fu, Stefan Ma, and Tee Hiang Cheng. "Effects of fear factors in disease propagation." Journal of Physics A: Mathematical and Theoretical 44, no. 35 (August 9, 2011): 355101. http://dx.doi.org/10.1088/1751-8113/44/35/355101.

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12

Xu, Zhiting. "Wave propagation in an infectious disease model." Journal of Mathematical Analysis and Applications 449, no. 1 (May 2017): 853–71. http://dx.doi.org/10.1016/j.jmaa.2016.11.051.

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13

Zhai, Bo, and Zhi Min Gong. "Numerical Simulation Modeling of GPR on Road Disease." Applied Mechanics and Materials 178-181 (May 2012): 1463–68. http://dx.doi.org/10.4028/www.scientific.net/amm.178-181.1463.

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Numerical simulation of ground penetrating radar is an effective way of analyzing and studying high frequency electromagnetic wave propagation rules in the underground media. In this paper, Finite-Difference Time-Domain (FDTD) method is used for numerical simulation to form radar records reflection profile about road disease such as loose disease. The purpose is to study and sum up the radar wave propagation rules and reflection signal characters in this diseases media, in order to provide reliable theory support for road maintenance and evaluation.

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14

Liu, Renming, Christopher A. Mancuso, Anna Yannakopoulos, Kayla A. Johnson, and Arjun Krishnan. "Supervised learning is an accurate method for network-based gene classification." Bioinformatics 36, no. 11 (April 14, 2020): 3457–65. http://dx.doi.org/10.1093/bioinformatics/btaa150.

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Abstract Background Assigning every human gene to specific functions, diseases and traits is a grand challenge in modern genetics. Key to addressing this challenge are computational methods, such as supervised learning and label propagation, that can leverage molecular interaction networks to predict gene attributes. In spite of being a popular machine-learning technique across fields, supervised learning has been applied only in a few network-based studies for predicting pathway-, phenotype- or disease-associated genes. It is unknown how supervised learning broadly performs across different networks and diverse gene classification tasks, and how it compares to label propagation, the widely benchmarked canonical approach for this problem. Results In this study, we present a comprehensive benchmarking of supervised learning for network-based gene classification, evaluating this approach and a classic label propagation technique on hundreds of diverse prediction tasks and multiple networks using stringent evaluation schemes. We demonstrate that supervised learning on a gene’s full network connectivity outperforms label propagaton and achieves high prediction accuracy by efficiently capturing local network properties, rivaling label propagation’s appeal for naturally using network topology. We further show that supervised learning on the full network is also superior to learning on node embeddings (derived using node2vec), an increasingly popular approach for concisely representing network connectivity. These results show that supervised learning is an accurate approach for prioritizing genes associated with diverse functions, diseases and traits and should be considered a staple of network-based gene classification workflows. Availability and implementation The datasets and the code used to reproduce the results and add new gene classification methods have been made freely available. Contact arjun@msu.edu Supplementary information Supplementary data are available at Bioinformatics online.

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15

Clarke, Anthony R., Graham S. Jackson, and John Collinge. "The molecular biology of prion propagation." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1406 (February 28, 2001): 185–95. http://dx.doi.org/10.1098/rstb.2000.0764.

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Prion diseases such as Creutzfeldt–Jakob disease (CJD) in humans and scrapie and bovine spongiform encephalopathy (BSE) in animals are associated with the accumulation in affected brains of a conformational isomer (PrP Sc ) of host–derived prion protein (PrP C ). According to the protein–only hypothesis, PrP Sc is the principal or sole component of transmissible prions. The conformational change known to be central to prion propagation, from a predominantly α–helical fold to one predominantly comprising β structure, can now be reproduced in vitro , and the ability of β–PrP to form fibrillar aggregates provides a plausible molecular mechanism for prion propagation. The existence of multiple prion strains has been difficult to explain in terms of a protein–only infectious agent but recent studies of human prion diseases suggest that strain–specific phenotypes can be encoded by different PrP conformations and glycosylation patterns. The experimental confirmation that a novel form of human prion disease, variant CJD, is caused by the same prion strain as cattle BSE, has highlighted the pressing need to understand the molecular basis of prion propagation and the transmission barriers that limit their passage between mammalian species. These and other advances in the fundamental biology of prion propagation are leading to strategies for the development of rational therapeutics.

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16

Rossi, Marcello, Simone Baiardi, and Piero Parchi. "Understanding Prion Strains: Evidence from Studies of the Disease Forms Affecting Humans." Viruses 11, no. 4 (March 29, 2019): 309. http://dx.doi.org/10.3390/v11040309.

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Prion diseases are a unique group of rare neurodegenerative disorders characterized by tissue deposition of heterogeneous aggregates of abnormally folded protease-resistant prion protein (PrPSc), a broad spectrum of disease phenotypes and a variable efficiency of disease propagation in vivo. The dominant clinicopathological phenotypes of human prion disease include Creutzfeldt–Jakob disease, fatal insomnia, variably protease-sensitive prionopathy, and Gerstmann–Sträussler–Scheinker disease. Prion disease propagation into susceptible hosts led to the isolation and characterization of prion strains, initially operatively defined as “isolates” causing diseases with distinctive characteristics, such as the incubation period, the pattern of PrPSc distribution, and the regional severity of neuropathological changes after injection into syngeneic hosts. More recently, the structural basis of prion strains has been linked to amyloid polymorphs (i.e., variant amyloid protein conformations) and the concept extended to all protein amyloids showing polymorphic structures and some evidence of in vivo or in vitro propagation by seeding. Despite the significant advances, however, the link between amyloid structure and disease is not understood in many instances. Here we reviewed the most significant contributions of human prion disease studies to current knowledge of the molecular basis of phenotypic variability and the prion strain phenomenon and underlined the unsolved issues from the human disease perspective.

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17

Sarell, Claire J., Emma Quarterman, Daniel C. M. Yip, Cassandra Terry, Andrew J. Nicoll, Jonathan D. F. Wadsworth, Mark A. Farrow, Dominic M. Walsh, and John Collinge. "Soluble Aβ aggregates can inhibit prion propagation." Open Biology 7, no. 11 (November 2017): 170158. http://dx.doi.org/10.1098/rsob.170158.

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Mammalian prions cause lethal neurodegenerative diseases such as Creutzfeldt–Jakob disease (CJD) and consist of multi-chain assemblies of misfolded cellular prion protein (PrP C ). Ligands that bind to PrP C can inhibit prion propagation and neurotoxicity. Extensive prior work established that certain soluble assemblies of the Alzheimer's disease (AD)-associated amyloid β-protein (Aβ) can tightly bind to PrP C , and that this interaction may be relevant to their toxicity in AD. Here, we investigated whether such soluble Aβ assemblies might, conversely, have an inhibitory effect on prion propagation. Using cellular models of prion infection and propagation and distinct Aβ preparations, we found that the form of Aβ assemblies which most avidly bound to PrP in vitro also inhibited prion infection and propagation. By contrast, forms of Aβ which exhibit little or no binding to PrP were unable to attenuate prion propagation. These data suggest that soluble aggregates of Aβ can compete with prions for binding to PrP C and emphasize the bidirectional nature of the interplay between Aβ and PrP C in Alzheimer's and prion diseases. Such inhibitory effects of Aβ on prion propagation may contribute to the apparent fall-off in the incidence of sporadic CJD at advanced age where cerebral Aβ deposition is common.

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18

Barengo, Marika, Isabella Iennaco, and Ezio Venturino. "The consequences of habitat fragmentation on disease propagation." International Journal of Computer Mathematics 91, no. 6 (September 9, 2013): 1202–23. http://dx.doi.org/10.1080/00207160.2013.829212.

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19

Dagher, Alain, and Yashar Zeighami. "Testing the Protein Propagation Hypothesis of Parkinson Disease." Journal of Experimental Neuroscience 12 (January 2018): 117906951878671. http://dx.doi.org/10.1177/1179069518786715.

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20

Moreno, Julie A., and Glenn C. Telling. "Molecular Mechanisms of Chronic Wasting Disease Prion Propagation." Cold Spring Harbor Perspectives in Medicine 8, no. 6 (February 13, 2017): a024448. http://dx.doi.org/10.1101/cshperspect.a024448.

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21

GAO, SHUJING, YUMIN DING, and JIANPING XIE. "ROLE OF DISEASE PROPAGATION IN MIGRATORY BIRD POPULATION." International Journal of Biomathematics 05, no. 03 (May 2012): 1260002. http://dx.doi.org/10.1142/s1793524512600029.

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Chatterjee considered a predator–prey model with avian migration in the migration prey population [S. Chatterjee, Alternative prey source coupled with prey recovery enhance stability between migratory prey and their predator in the presence of disease, Nonlinear Anal. Real World Appl. 11 (2010) 4415–4430]. In this paper, we modify and analyze the model by taking time dependent parameters and the general functional response into consideration. The conditions for the persistence of the system and the extinction of the disease are obtained. The global attractivity of the system is also studied. By numerical simulations, we find that the qualitative behavior of the system independent on the choice of the functional response. Moreover, it is observed that the infection rate, recruitment rate and the predation rate play a vital role in predicting the behavior of the dynamics.

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22

Jackson, Graham S., and John Collinge. "Prion disease – the propagation of infectious protein topologies." Microbes and Infection 2, no. 12 (October 2000): 1445–49. http://dx.doi.org/10.1016/s1286-4579(00)01299-5.

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23

Picart-Armada, Sergio, Steven J. Barrett, David R. Willé, Alexandre Perera-Lluna, Alex Gutteridge, and Benoit H. Dessailly. "Benchmarking network propagation methods for disease gene identification." PLOS Computational Biology 15, no. 9 (September 3, 2019): e1007276. http://dx.doi.org/10.1371/journal.pcbi.1007276.

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24

Piqueira, José Roberto C. "Rumor Propagation Model: An Equilibrium Study." Mathematical Problems in Engineering 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/631357.

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Compartmental epidemiological models have been developed since the 1920s and successfully applied to study the propagation of infectious diseases. Besides, due to their structure, in the 1960s an interesting version of these models was developed to clarify some aspects of rumor propagation, considering that spreading an infectious disease or disseminating information is analogous phenomena. Here, in an analogy with the SIR (Susceptible-Infected-Removed) epidemiological model, the ISS (Ignorant-Spreader-Stifler) rumor spreading model is studied. By using concepts from the Dynamical Systems Theory, stability of equilibrium points is established, according to propagation parameters and initial conditions. Some numerical experiments are conducted in order to validate the model.

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25

Acquatella-Tran Van Ba, Isabelle, Thibaut Imberdis, and Véronique Perrier. "From Prion Diseases to Prion-Like Propagation Mechanisms of Neurodegenerative Diseases." International Journal of Cell Biology 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/975832.

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Prion diseases are fatal neurodegenerative sporadic, inherited, or acquired disorders. In humans, Creutzfeldt-Jakob disease is the most studied prion disease. In animals, the most frequent prion diseases are scrapie in sheep and goat, bovine spongiform encephalopathy in cattle, and the emerging chronic wasting disease in wild and captive deer in North America. The hallmark of prion diseases is the deposition in the brain of PrPSc, an abnormalβ-sheet-rich form of the cellular prion protein (PrPC) (Prusiner 1982). According to the prion hypothesis, PrPSccan trigger the autocatalytic conversion of PrPCinto PrPSc, presumably in the presence of cofactors (lipids and small RNAs) that have been recently identified. In this review, we will come back to the original works that led to the discovery of prions and to the protein-only hypothesis proposed by Dr. Prusiner. We will then describe the recent reports on mammalian synthetic prions and recombinant prions that strongly support the protein-only hypothesis. The new concept of “deformed templating” regarding a new mechanism of PrPScformation and replication will be exposed. The review will end with a chapter on the prion-like propagation of other neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease and tauopathies.

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26

Razik, A., A. Grinstein, and J. Katan. "RHIZOCTONIA DISEASE IN PROPAGATION MATERIAL AND FIELD GROWN STRAWBERRY." Acta Horticulturae, no. 265 (December 1989): 579–85. http://dx.doi.org/10.17660/actahortic.1989.265.86.

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27

Martin, C. W. "ROSE ROSETTE DISEASE AND THE IMPACTS ON PROPAGATION©." Acta Horticulturae, no. 1055 (October 2014): 319–21. http://dx.doi.org/10.17660/actahortic.2014.1055.68.

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28

Hansen, Christian, and Jia-Yi Li. "Beyond α-synuclein transfer: pathology propagation in Parkinson's disease." Trends in Molecular Medicine 18, no. 5 (May 2012): 248–55. http://dx.doi.org/10.1016/j.molmed.2012.03.002.

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29

Casciola-Rosen, Livia. "Autoimmune myositis: new concepts for disease initiation and propagation." Current Opinion in Rheumatology 17, no. 6 (November 2005): 699–700. http://dx.doi.org/10.1097/01.bor.0000179940.14109.50.

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30

Hijazi, Nuha, Yuval Shaked, Hana Rosenmann, Tamir Ben-Hur, and Ruth Gabizon. "Copper binding to PrPC may inhibit prion disease propagation." Brain Research 993, no. 1-2 (December 2003): 192–200. http://dx.doi.org/10.1016/j.brainres.2003.09.014.

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31

Faragó, István, and Róbert Horváth. "Qualitative properties of some discrete models of disease propagation." Journal of Computational and Applied Mathematics 340 (October 2018): 486–500. http://dx.doi.org/10.1016/j.cam.2017.09.024.

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32

Kordower, Jeffrey H., and Patrik Brundin. "Propagation of host disease to grafted neurons: Accumulating evidence." Experimental Neurology 220, no. 2 (December 2009): 224–25. http://dx.doi.org/10.1016/j.expneurol.2009.09.016.

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33

Wade, R., L. Igali, and A. Figus. "Skin involvement in Dupuytren’s disease." Journal of Hand Surgery (European Volume) 41, no. 6 (September 9, 2015): 600–608. http://dx.doi.org/10.1177/1753193415601353.

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Whether the palmar skin has a role in the development, propagation or recurrence of Dupuytren’s disease remains unclear. Clinical assessment for skin involvement is difficult and its correlation with histology uncertain. We prospectively biopsied the palmar skin of consecutive patients undergoing single digit fasciectomy (for primary Dupuytren’s disease without clinically involved skin) and dermofasciectomy (for clinically involved skin or recurrence) in order to investigate this relationship. We found dermal fibromatosis in 22 of 44 patients (50%) undergoing fasciectomy and 41 of 59 patients (70%) undergoing dermofasciectomy. Dermal fibromatosis appeared to be associated with greater preoperative angular deformity, presence of palmar nodules and occupations involving manual labour. Dermal fibromatosis exists in the absence of clinical features of skin involvement and we hypothesize that the skin may have a greater role in the development and propagation of Dupuytren’s disease than previously thought. Level of evidence: III

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Turechek, W. W. "Spatial Distribution of Crown Gall in a Commercial Nursery of Weeping Fig." Plant Health Progress 13, no. 1 (January 2012): 3. http://dx.doi.org/10.1094/php-2012-1126-01-rs.

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Agrobacterium larrymoorei causes tumors on weeping fig. The association between propagation and pathogen spread in mother trees and daughter branches was studied in a commercial nursery. The mother tree planting was scouted for tumors prior to and after propagation. Branches selected for propagation were tagged to track disease development. The spatial distribution of crown gall in the mother tree planting was characterized with runs, join-count, and spatial autocorrelation analyses. The association of disease in mother trees and daughter branches was characterized with cross-correlation analysis. The incidence of crown gall in the mother tree planting increased from 7% prior to propagation to 32% eight months after propagation. Of the 4193 daughter branches monitored, 3.8% developed tumors. Runs analysis indicated significant clustering of diseased mother trees. Significant cross-correlations between mother trees and daughter branches with symptoms of crown gall were detected out to a distance of two plants from the source. Although pruning shears were routinely soaked in a disinfectant in this nursery, the degree of sterilization achieved apparently was not sufficient to prevent pathogen transmission. This study suggests that alternative sanitation measures should be sought and that infected mother trees and their neighbors should be avoided for propagation. Accepted for publication 5 November 2012. Published 26 November 2012.

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Kaufmann, Dan, Jeremy J. Theriot, Jekaterina Zyuzin, C. Austin Service, Joshua C. Chang, Y. Tanye Tang, Vladimir B. Bogdanov, et al. "Heterogeneous incidence and propagation of spreading depolarizations." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (October 1, 2016): 1748–62. http://dx.doi.org/10.1177/0271678x16659496.

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Spreading depolarizations are implicated in a diverse set of neurologic diseases. They are unusual forms of nervous system activity in that they propagate very slowly and approximately concentrically, apparently not respecting the anatomic, synaptic, functional, or vascular architecture of the brain. However, there is evidence that spreading depolarizations are not truly concentric, isotropic, or homogeneous, either in space or in time. Here we present evidence from KCl-induced spreading depolarizations, in mouse and rat, in vivo and in vitro, showing the great variability that these depolarizations can exhibit. This variability can help inform the mechanistic understanding of spreading depolarizations, and it has implications for their phenomenology in neurologic disease.

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Caughey, Byron, and Allison Kraus. "Transmissibility versus Pathogenicity of Self-Propagating Protein Aggregates." Viruses 11, no. 11 (November 9, 2019): 1044. http://dx.doi.org/10.3390/v11111044.

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The prion-like spreading and accumulation of specific protein aggregates appear to be central to the pathogenesis of many human diseases, including Alzheimer’s and Parkinson’s. Accumulating evidence indicates that inoculation of tissue extracts from diseased individuals into suitable experimental animals can in many cases induce the aggregation of the disease-associated protein, as well as related pathological lesions. These findings, together with the history of the prion field, have raised the questions about whether such disease-associated protein aggregates are transmissible between humans by casual or iatrogenic routes, and, if so, do they propagate enough in the new host to cause disease? These practical considerations are important because real, and perhaps even only imagined, risks of human-to-human transmission of diseases such as Alzheimer’s and Parkinson’s may force costly changes in clinical practice that, in turn, are likely to have unintended consequences. The prion field has taught us that a single protein, PrP, can aggregate into forms that can propagate exponentially in vitro, but range from being innocuous to deadly when injected into experimental animals in ways that depend strongly on factors such as conformational subtleties, routes of inoculation, and host responses. In assessing the hazards posed by various disease-associated, self-propagating protein aggregates, it is imperative to consider both their actual transmissibilities and the pathological consequences of their propagation, if any, in recipient hosts.

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Warner, Fiona J., Harinda Rajapaksha, Nicholas Shackel, and Chandana B. Herath. "ACE2: from protection of liver disease to propagation of COVID-19." Clinical Science 134, no. 23 (December 2020): 3137–58. http://dx.doi.org/10.1042/cs20201268.

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Abstract Twenty years ago, the discovery of angiotensin-converting enzyme 2 (ACE2) was an important breakthrough dramatically enhancing our understanding of the renin–angiotensin system (RAS). The classical RAS is driven by its key enzyme ACE and is pivotal in the regulation of blood pressure and fluid homeostasis. More recently, it has been recognised that the protective RAS regulated by ACE2 counterbalances many of the deleterious effects of the classical RAS. Studies in murine models demonstrated that manipulating the protective RAS can dramatically alter many diseases including liver disease. Liver-specific overexpression of ACE2 in mice with liver fibrosis has proved to be highly effective in antagonising liver injury and fibrosis progression. Importantly, despite its highly protective role in disease pathogenesis, ACE2 is hijacked by SARS-CoV-2 as a cellular receptor to gain entry to alveolar epithelial cells, causing COVID-19, a severe respiratory disease in humans. COVID-19 is frequently life-threatening especially in elderly or people with other medical conditions. As an unprecedented number of COVID-19 patients have been affected globally, there is an urgent need to discover novel therapeutics targeting the interaction between the SARS-CoV-2 spike protein and ACE2. Understanding the role of ACE2 in physiology, pathobiology and as a cellular receptor for SARS-CoV-2 infection provides insight into potential new therapeutic strategies aiming to prevent SARS-CoV-2 infection related tissue injury. This review outlines the role of the RAS with a strong focus on ACE2-driven protective RAS in liver disease and provides therapeutic approaches to develop strategies to prevent SARS-CoV-2 infection in humans.

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38

Ning, Yi-zi. "Effects of epidemic prevention on the university management." Advances in Social Sciences Research Journal 7, no. 10 (November 3, 2020): 311–16. http://dx.doi.org/10.14738/assrj.710.9211.

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The information transmission network is different from the physical contact network. It is of great significance to study the spread range of epidemic diseases by distinguishing the topological structure of perceptual information transmission network from that of physical contact disease diffusion network. SIR model is used to describe the transmission process of epidemic, and it is very important to explore the disease diffusion model which integrates perceptual transmission and disease diffusion. Furthermore, with a multi-layer network coupling the diffusion of perceptual information and the spread of disease, the relationship between different layers is the key element of the system model. Using multi-layer network to describe the system in the real world, through the introduction of individual awareness propagation mechanism, this paper studies the interaction between epidemic diffusion and awareness propagation in the framework of multiple networks, and establishes multiple policy adjustment rules to study the propagation dynamics of awareness in different networks. Considering the two-layer network, the first layer network is described as physical contact network, and epidemic diseases spread through the physical contact network, which affects the mutual transmission of information at the level of awareness network. The other layer is awareness communication network. It is an important task to study the complex interaction between human society and biological infectious diseases. In this work, we study the influence of awareness and behavior based on multiple networks on infection density. The university management should pay attention to topological structures of networks and the strategies.

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39

Marciniuk, Kristen, Ryan Taschuk, and Scott Napper. "Evidence for Prion-Like Mechanisms in Several Neurodegenerative Diseases: Potential Implications for Immunotherapy." Clinical and Developmental Immunology 2013 (2013): 1–20. http://dx.doi.org/10.1155/2013/473706.

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Transmissible spongiform encephalopathies (TSEs) are fatal, untreatable neurodegenerative diseases. While the impact of TSEs on human health is relatively minor, these diseases are having a major influence on how we view, and potentially treat, other more common neurodegenerative disorders. Until recently, TSEs encapsulated a distinct category of neurodegenerative disorder, exclusive in their defining characteristic of infectivity. It now appears that similar mechanisms of self-propagation may underlie other proteinopathies such as Alzheimer’s disease, Parkinson’s disease, Amyotrophic lateral sclerosis, and Huntington’s disease. This link is of scientific interest and potential therapeutic importance as this route of self-propagation offers conceptual support and guidance for vaccine development efforts. Specifically, the existence of a pathological, self-promoting isoform offers a rational vaccine target. Here, we review the evidence of prion-like mechanisms within a number of common neurodegenerative disorders and speculate on potential implications and opportunities for vaccine development.

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Pasini, C., and M. G. Fantino. "CONTROL OF FUSARIUM DISEASE IN IXIA BY DIPPING PROPAGATION MATERIAL." Acta Horticulturae, no. 266 (March 1990): 407–12. http://dx.doi.org/10.17660/actahortic.1990.266.54.

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Wang, Xiang-Sheng, Haiyan Wang, and Jianhong Wu. "Traveling waves of diffusive predator-prey systems: Disease outbreak propagation." Discrete & Continuous Dynamical Systems - A 32, no. 9 (2012): 3303–24. http://dx.doi.org/10.3934/dcds.2012.32.3303.

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Kobayashi, Shunsuke, Yuko Saito, Toshiyuki Maki, and Shigeo Murayama. "Cortical propagation of Creutzfeldt–Jakob disease with codon 180 mutation." Clinical Neurology and Neurosurgery 112, no. 6 (July 2010): 520–23. http://dx.doi.org/10.1016/j.clineuro.2010.03.015.

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Tirado-Ramos, Alfredo, and Chris Kelley. "Next Steps in Simulating High-risk Infectious Disease Propagation Networks." Procedia Computer Science 18 (2013): 1421–28. http://dx.doi.org/10.1016/j.procs.2013.05.309.

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Duyckaerts, Charles, Florence Clavaguera, and Marie-Claude Potier. "The prion-like propagation hypothesis in Alzheimerʼs and Parkinsonʼs disease." Current Opinion in Neurology 32, no. 2 (April 2019): 266–71. http://dx.doi.org/10.1097/wco.0000000000000672.

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Andrade-Restrepo, Martin, Paul Lemarre, Laurent Pujo-Menjouet, Leon Matar Tine, and Sorin Ionel Ciuperca. "Modeling the spatial propagation of Aβ oligomers in Alzheimer’s Disease." ESAIM: Proceedings and Surveys 67 (2020): 30–45. http://dx.doi.org/10.1051/proc/202067003.

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Recent advances in the study of Alzheimer’s Disease and the role of Aβ amyloid formation have caused the focus of biologists to progressively shift towards the smaller protein assemblies, the oligomers. These appear very early on in the disease progression and they seem to be the most infectious species for the neurons. We suggest a model of spatial propagation of Aβ oligomers in the vicinity of a few neurons, without considering the formation of large ﬁbrils or plaques. We also include a simple representation of the oligomers neurotoxic effect. A numerical study reveals that the oligomers spatial dynamics are very sensitive to the balance between their diffusion and their replication, and that the outcome in terms of the progression of AD strongly depends on it.

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Zheng, Ying-Qiu, Yu Zhang, Yvonne Yau, Yashar Zeighami, Kevin Larcher, Bratislav Misic, and Alain Dagher. "Local vulnerability and global connectivity jointly shape neurodegenerative disease propagation." PLOS Biology 17, no. 11 (November 21, 2019): e3000495. http://dx.doi.org/10.1371/journal.pbio.3000495.

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Fast, Shannon M., Marta C. González, James M. Wilson, and Natasha Markuzon. "Modelling the propagation of social response during a disease outbreak." Journal of The Royal Society Interface 12, no. 104 (March 2015): 20141105. http://dx.doi.org/10.1098/rsif.2014.1105.

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Epidemic trajectories and associated social responses vary widely between populations, with severe reactions sometimes observed. When confronted with fatal or novel pathogens, people exhibit a variety of behaviours from anxiety to hoarding of medical supplies, overwhelming medical infrastructure and rioting. We developed a coupled network approach to understanding and predicting social response. We couple the disease spread and panic spread processes and model them through local interactions between agents. The social contagion process depends on the prevalence of the disease, its perceived risk and a global media signal. We verify the model by analysing the spread of disease and social response during the 2009 H1N1 outbreak in Mexico City and 2003 severe acute respiratory syndrome and 2009 H1N1 outbreaks in Hong Kong, accurately predicting population-level behaviour. This kind of empirically validated model is critical to exploring strategies for public health intervention, increasing our ability to anticipate the response to infectious disease outbreaks.

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Vanunu, Oron, Oded Magger, Eytan Ruppin, Tomer Shlomi, and Roded Sharan. "Associating Genes and Protein Complexes with Disease via Network Propagation." PLoS Computational Biology 6, no. 1 (January 15, 2010): e1000641. http://dx.doi.org/10.1371/journal.pcbi.1000641.

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Ramirez, Marianela, Marek J. Krasowski, and Judy A. Loo. "Vegetative Propagation of American Beech Resistant to Beech Bark Disease." HortScience 42, no. 2 (April 2007): 320–24. http://dx.doi.org/10.21273/hortsci.42.2.320.

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The objective of this study was to develop vegetative propagation techniques—using tissue culture and grafting—for American beech (Fagus grandifolia) resistant to beech bark disease. Resterilizing the buds after excising bud scales reduced contamination of in vitro cultures derived from dormant buds. Application of a 7-day dark treatment before transferring shoots to the rooting medium improved rooting success. Plantlets gradually acclimatized to nonsterile growth conditions and set buds but failed to survive the dormant period. The application of 6-benzyladenine enhanced sprouting from roots collected from mature trees, but the excised shoots rooted poorly in vitro despite low contamination. Success of grafting scions from mature trees varied among genotypes and differed each year (30% in 2003, 12% in 2004, and 18% in 2005). Applying the growth hormone indole butyric acid to the scion before joining it to the rootstock did not increase grafting success. Survival of grafts was independent of rootstock age (1 or 2 years old). Grafting success increased when scion diameter was slightly larger than rootstock diameter. The rooting of sucker cuttings was successful for only one genotype. Critical steps, in which most failures in the propagation of American beech occur, are identified.

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Radhimeenakshi, S., and G. M. Nasira. "Prediction of Heart Disease using Neural Network with Back Propagation." International Journal of Data Mining Techniques and Applications 4, no. 1 (June 15, 2015): 19–22. http://dx.doi.org/10.20894/ijdmta.102.004.001.005.

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