Pub Date : 2013-01-01DOI: 10.1016/S1405-888X(13)72079-5
Ivonne Domínguez , Rafael A. Barrio , Carmen Varea , José Luis Aragón
In cardiac electrical activity, different types of waves meander through the heart. We present a model of the electrical activity of the heart that proposes that the homogeneous wave fronts propagating through the heart are in fact solitons. We use a general set of reaction-diffusion equations known as the Barrio-Varea-Aragón-Maini (BVAM) model[1] that presents a wealth of non-linear bifurcations, and we are able to follow the route to chaos, using a mapping of the amplitude equations to the dynamics of the complex Ginzburg-Landau equation. We study the dynamics of wave fronts numerically in the BVAM model to describe the mechanisms leading to heart fibrillation and compare the findings with experimental data.
{"title":"Modelo de propagación de ondas solitarias en el corazón","authors":"Ivonne Domínguez , Rafael A. Barrio , Carmen Varea , José Luis Aragón","doi":"10.1016/S1405-888X(13)72079-5","DOIUrl":"10.1016/S1405-888X(13)72079-5","url":null,"abstract":"<div><p>In cardiac electrical activity, different types of waves meander through the heart. We present a model of the electrical activity of the heart that proposes that the homogeneous wave fronts propagating through the heart are in fact solitons. We use a general set of reaction-diffusion equations known as the Barrio-Varea-Aragón-Maini (BVAM) model<sup>[</sup><sup>1</sup><sup>]</sup> that presents a wealth of non-linear bifurcations, and we are able to follow the route to chaos, using a mapping of the amplitude equations to the dynamics of the complex Ginzburg-Landau equation. We study the dynamics of wave fronts numerically in the BVAM model to describe the mechanisms leading to heart fibrillation and compare the findings with experimental data.</p></div>","PeriodicalId":31507,"journal":{"name":"TIP Revista Especializada en Ciencias QuimicoBiologicas","volume":"16 2","pages":"Pages 79-92"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1405-888X(13)72079-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74063860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01DOI: 10.1016/S1405-888X(13)72082-5
Magda Carvajal
Aflatoxins (AF) are secondary toxic metabolites formed mainly by the molds Aspergillus flavus and A. parasiticus; they are potent mutagens and carcinogens of foods, and human exposure to them is continuous. AF bind to DNA, RNA and proteins forming AFB1-DNA adducts that accumulate for years and damage from viruses to humans. To identify and quantify the chemical reactions and molecular biology of these adducts is of primary importance because they are long-term biomarkers validated as a source of mutagenicity and risk of cancer in animals and humans. The cytochrome P450 activates AF as an unstable molecule called 8,9 AFB1 epoxide, that binds mainly to the N7 of the guanine nucleotide forming adducts that are the active carcinogens themselves and, as biomarkers, an objective measure of human exposure to environmental carcinogens. Adducts represent an integration of exposure, absorption, distribution, metabolism, DNA repair, and cell turnover. The different issues presented here are the formation of AFB1-DNA adducts, in vitro and in vivo studies, dietary AFB1 exposure, effects, development of human cancer and mutations in the p53 tumor suppressor gene, the effect of diet, routes of exposure, vitamins, kinds of AFB1-DNA adducts, methodology used for their study and their control.
{"title":"Transformación de la aflatoxina B1 de alimentos, en el cancerígeno humano, aducto AFB1-ADN","authors":"Magda Carvajal","doi":"10.1016/S1405-888X(13)72082-5","DOIUrl":"10.1016/S1405-888X(13)72082-5","url":null,"abstract":"<div><p>Aflatoxins (AF) are secondary toxic metabolites formed mainly by the molds <em>Aspergillus flavus</em> and <em>A. parasiticus</em>; they are potent mutagens and carcinogens of foods, and human exposure to them is continuous. AF bind to DNA, RNA and proteins forming AFB<sub>1</sub>-DNA adducts that accumulate for years and damage from viruses to humans. To identify and quantify the chemical reactions and molecular biology of these adducts is of primary importance because they are long-term biomarkers validated as a source of mutagenicity and risk of cancer in animals and humans. The cytochrome P<sub>450</sub> activates AF as an unstable molecule called 8,9 AFB<sub>1</sub> epoxide, that binds mainly to the N<sup>7</sup> of the guanine nucleotide forming adducts that are the active carcinogens themselves and, as biomarkers, an objective measure of human exposure to environmental carcinogens. Adducts represent an integration of exposure, absorption, distribution, metabolism, DNA repair, and cell turnover. The different issues presented here are the formation of AFB<sub>1</sub>-DNA adducts, in vitro and <em>in vivo</em> studies, dietary AFB<sub>1</sub> exposure, effects, development of human cancer and mutations in the p53 tumor suppressor gene, the effect of diet, routes of exposure, vitamins, kinds of AFB<sub>1</sub>-DNA adducts, methodology used for their study and their control.<span></span></p></div>","PeriodicalId":31507,"journal":{"name":"TIP Revista Especializada en Ciencias QuimicoBiologicas","volume":"16 2","pages":"Pages 109-120"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1405-888X(13)72082-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74117954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}