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1.
Phys Rev E ; 108(5-1): 054407, 2023 Nov.
Article de Anglais | MEDLINE | ID: mdl-38115402

RÉSUMÉ

Complex biological processes involve collective behavior of entities (bacteria, cells, animals) over many length and time scales and can be described by discrete models that track individuals or by continuum models involving densities and fields. We consider hybrid stochastic agent-based models of branching morphogenesis and angiogenesis (new blood vessel creation from preexisting vasculature), which treat cells as individuals that are guided by underlying continuous chemical and/or mechanical fields. In these descriptions, leader (tip) cells emerge from existing branches and follower (stalk) cells build the new sprout in their wake. Vessel branching and fusion (anastomosis) occur as a result of tip and stalk cell dynamics. Coarse graining these hybrid models in appropriate limits produces continuum partial differential equations (PDEs) for endothelial cell densities that are more analytically tractable. While these models differ in nonlinearity, they produce similar equations at leading order when chemotaxis is dominant. We analyze this leading order system in a simple quasi-one-dimensional geometry and show that the numerical solution of the leading order PDE is well described by a soliton wave that evolves from vessel to source. This wave is an attractor for intermediate times until it arrives at the hypoxic region releasing the growth factor. The mathematical techniques used here thus identify common features of discrete and continuum approaches and provide insight into general biological mechanisms governing their collective dynamics.


Sujet(s)
Chimiotaxie , Néovascularisation pathologique , Humains , Animaux , Modèles biologiques , Simulation numérique
2.
Phys Rev E ; 104(3-2): 035303, 2021 Sep.
Article de Anglais | MEDLINE | ID: mdl-34654121

RÉSUMÉ

Time periodic patterns in a semiconductor superlattice, relevant to microwave generation, are obtained upon numerical integration of a known set of drift-diffusion equations. The associated spatiotemporal transport mechanisms are uncovered by applying (to the computed data) two recent data processing tools, known as the higher order dynamic mode decomposition and the spatiotemporal Koopman decomposition. Outcomes include a clear identification of the asymptotic self-sustained oscillations of the current density (isolated from the transient dynamics) and an accurate description of the electric field traveling pulse in terms of its dispersion diagram. In addition, a preliminary version of a data-driven reduced order model is constructed, which allows for extremely fast online simulations of the system response over a range of different configurations.

3.
Sci Rep ; 6: 31296, 2016 08 09.
Article de Anglais | MEDLINE | ID: mdl-27503562

RÉSUMÉ

Angiogenesis is a multiscale process by which blood vessels grow from existing ones and carry oxygen to distant organs. Angiogenesis is essential for normal organ growth and wounded tissue repair but it may also be induced by tumours to amplify their own growth. Mathematical and computational models contribute to understanding angiogenesis and developing anti-angiogenic drugs, but most work only involves numerical simulations and analysis has lagged. A recent stochastic model of tumour-induced angiogenesis including blood vessel branching, elongation, and anastomosis captures some of its intrinsic multiscale structures, yet allows one to extract a deterministic integropartial differential description of the vessel tip density. Here we find that the latter advances chemotactically towards the tumour driven by a soliton (similar to the famous Korteweg-de Vries soliton) whose shape and velocity change slowly. Analysing these collective coordinates paves the way for controlling angiogenesis through the soliton, the engine that drives this process.


Sujet(s)
Inhibiteurs de l'angiogenèse/pharmacologie , Modèles cardiovasculaires , Néovascularisation pathologique , Animaux , Phénomènes physiologiques cardiovasculaires , Chimiotaxie , Humains , Tumeurs/traitement médicamenteux , Logiciel , Processus stochastiques
4.
Phys Rev E ; 93(2): 022413, 2016 Feb.
Article de Anglais | MEDLINE | ID: mdl-26986368

RÉSUMÉ

A recent conceptual model of tumor-driven angiogenesis including branching, elongation, and anastomosis of blood vessels captures some of the intrinsic multiscale structures of this complex system, yet allowing one to extract a deterministic integro-partial-differential description of the vessel tip density [Phys. Rev. E 90, 062716 (2014)]. Here we solve the stochastic model, show that ensemble averages over many realizations correspond to the deterministic equations, and fit the anastomosis rate coefficient so that the total number of vessel tips evolves similarly in the deterministic and ensemble-averaged stochastic descriptions.


Sujet(s)
Tumeurs/vascularisation , Néovascularisation pathologique , Modèles biologiques , Processus stochastiques
5.
Phys Rev E ; 94(6-1): 062415, 2016 Dec.
Article de Anglais | MEDLINE | ID: mdl-28085400

RÉSUMÉ

Recently, numerical simulations of a stochastic model have shown that the density of vessel tips in tumor-induced angiogenesis adopts a solitonlike profile [Sci. Rep. 6, 31296 (2016)2045-232210.1038/srep31296]. In this work, we derive and solve the equations for the soliton collective coordinates that indicate how the soliton adapts its shape and velocity to varying chemotaxis and diffusion. The vessel tip density can be reconstructed from the soliton formulas. While the stochastic model exhibits large fluctuations, we show that the location of the maximum vessel tip density for different replicas follows closely the soliton peak position calculated either by ensemble averages or by solving an alternative deterministic description of the density. The simple soliton collective coordinate equations may also be used to ascertain the response of the vessel network to changes in the parameters and thus to control it.


Sujet(s)
Vaisseaux sanguins/croissance et développement , Modèles biologiques , Néovascularisation pathologique/physiopathologie , Chimiotaxie , Diffusion
7.
Ann Ig ; 7(5): 369-81, 1995.
Article de Italien | MEDLINE | ID: mdl-8679179

RÉSUMÉ

Since foodborne diseases, especially those caused by bacteria, have become an increasingly important public health problem, the Authors conducted a survey in order to evaluate the organization of, and the intervention carried out by, six Public Health Services in the Lombardia region, after reports of foodborne diseases outbreaks. Lack of correct methodology was detected, not to mention the usual omission of epidemic curves and attack rates. Besides, too many microbiological tests were made and it took too much time to take care of and to report the outbreaks to Regional and National Health Authorities. Forty-one outbreaks were examined: 415 cases occurred (AR: 28.7%), most of which home-made food-related. In 25 outbreaks the suspected food vehicles were eggs or fish, but only 5 of them were confirmed by laboratory tests. Salmonella enterica, either serovar Eenteritidis or group D, appeared responsible for 26 of the outbreaks [corrected].


Sujet(s)
Services de santé communautaires , Épidémies de maladies , Maladies d'origine alimentaire/épidémiologie , Sujet âgé , Enfant , Méthodes épidémiologiques , Maladies d'origine alimentaire/diagnostic , Maladies d'origine alimentaire/étiologie , Humains , Italie/épidémiologie , Facteurs de risque , Toxi-infection alimentaire à Salmonella/diagnostic , Toxi-infection alimentaire à Salmonella/épidémiologie , Enquêtes et questionnaires
8.
Cancer Detect Prev ; 17(2): 317-21, 1993.
Article de Anglais | MEDLINE | ID: mdl-8402719

RÉSUMÉ

Should we set any limits on patenting? More specifically, must we set any limits on patenting in the field of biotechnology? There should be general agreement on the exclusion of humans from patentability. The European Parliament voted unanimously on an amendment to the Community Directive regarding patenting stating that the human body and its parts are not patentable as such. Patenting of humans indeed would be against fundamental human rights; against the shared principles of freedom, autonomy, and dignity of each single human being. The same reasons apply to requests to reject the "commercialization of the human body." However, much more difficult is reaching a consensus on what are the parts of humans that should not be marketed--organs, tissues, cells, genes, smaller DNA fragments? Probably there is no consensus on where to draw the line when we deal with parts of the human body. Nevertheless, an ethical component is very strong in raising opposition to patenting human DNA. Whatever our personal view on the issue, we cannot deny that ethical aspects must be considered in granting patents on human DNA. With reference to animals, the fears raised are that the patenting of transgenic animals could amplify the instrumental use (reification) and the neglect of their sentient nonobjectual nature: patenting could motivate, instead, the tendency to consider animals as the standard of things invented and as new consumer products. Moreover, animal patenting increases production and thus brings about the great suffering of animals. In regard to plants, the ethical implications of patenting have more to do with their socioeconomic effects, in particular on Third World countries, than for the organisms involved.(ABSTRACT TRUNCATED AT 250 WORDS)


Sujet(s)
Biotechnologie , Éthique , Corps humain , Brevets comme sujet/législation et jurisprudence , Animaux , Animal génétiquement modifié , Recherche biomédicale , Europe , Génome humain , Humains , Internationalité , Plantes , Appréciation des risques , États-Unis
9.
Blood ; 68(3): 646-51, 1986 Sep.
Article de Anglais | MEDLINE | ID: mdl-2427137

RÉSUMÉ

We report a new type of deletion of the beta globin gene cluster in the Italian population that confers a phenotype of hereditary persistence of fetal hemoglobin (HPFH) to the carriers. This deletion begins approximately 5 kilobases (kb) 5' to the delta globin gene and ends approximately 30 kb 3' to the beta globin gene, in close proximity to the 3' end of an Indian HPFH. In all four previously described HPFH, a repetitive Alu I region 5' to the delta globin gene is largely or completely deleted; the 5' end of the new HPFH is consistent with this common feature. In addition, the finding that Italian and Indian HPFHs, as reported for other groups of deletions, have very close 3' ends, strengthens the idea that common mechanisms may operate in generating these deletions. Finally, we show that, in spite of similar 5' breakpoints, the deletion of Spanish delta beta(0)-thalassemia is at least 8 kb longer than that of Negro HPFH type I, thus ruling out the hypothesis that the overall extent of the deletion might influence the level of gamma globin chain synthesis.


Sujet(s)
Hémoglobine foetale/génétique , Globines/génétique , Hémoglobines anormales/génétique , Délétion de segment de chromosome , Cartographie chromosomique , DNA restriction enzymes , Humains , Italie
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