Search

This paper critically analyzes the book El ADN dictador. Lo que la genética decide por ti, written by the geneticist Miguel Pita. The book offers a radical defense of gene-centrism, which is taken to be the only available approach to the problem of causality of traits. However, gene-centrism is being challenged by developmentalism (a framework not even mentioned by Pita). This article discusses several gene-centric theses defended by the book and shows a developmentalism alternative to them. [ABSTRACT FROM AUTHOR]

Copyright of Biomédica: Revista del Instituto Nacional de Salud is the property of Instituto Nacional de Salud of Colombia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Salud Mental is the property of Instituto Nacional de Psiquiatria Ramon de la Fuente and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Estudios Socio-Jurídicos is the property of Colegio Mayor de Nuestra Senora del Rosario and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Human Review is the property of Eagora Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of the Selva Andina Animal Science is the property of Fundacion Selva Andina Research Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This paper describes an optimization process implemented using Genetic Algorithms. The initial population of the GA is composed of 128 chromosomes with 11 genes per chromosome. The chromosomes of the GA are composed by the length and separations of the elements of the Yagi-Uda antenna; the ranks of this genes where chosen by design standards for such antennas. All genes undergo a process of analysis to assess every one of the antennas of each generation of the GA to assign the fitness of the individuals. In order to verify the obtained results, various tests were made, and among them excel the construction of the optimized Yagi-Uda antenna to measure and verify it electromagnetic characteristics. [ABSTRACT FROM AUTHOR]

The interaction between genetic and environmental risk explain many aspects of the atherosclerosis and the genetic variations constitute markers of risk for the coronary disease, one of the main leading causes of death worldwide. The familiar predisposition to suffer coronary disease, combined with vertiginous advance in DNA analysis techniques and the availability of human genome sequences, has lead to the research of genetic alterations related to development of coronary disease. Because the coronary disease directly is related to alterations in the plasma lipid levels, the main effort in genetic research of coronary disease is directed to the identification of mutations or polymorphisms in genes involved in lipoprotein synthesis, transport and metabolism. The alterations in some genes candidates, such as R-LDL, apo-B100, apo-E, LPA, LPL, LH, CETP , apoAI, apoAII and LCAT have been well characterized, demonstrating its association to risk coronary disease in different populations. The genetic studies not only allow to define the contribution of genes alterations in the development of the coronary disease phenotype, but also to improve the understanding of their physiopathology and to define new alternatives of treatment through the identification of new molecules and possible therapeutic targets. In this paper the genetic predisposition to development dislipidaemia and the polymorphisms and mutations potentially implicated in the mechanisms of coronary disease are discussed. Genotype/phenotype, gene-gene and gene-environmental interactions related to lipid metabolism. Individual coronary risk might be related to the presence of a critical accumulation of detrimental polymorphisms. [ABSTRACT FROM AUTHOR]

Anew method to solve the branching problem in surfaces of three-dimensional (3D) models reconstructed from parallel cross sections is presented in this paper. This is an important problem in medical imaging and others object-modeling applications, where the reconstruction of the surface of 3D models from images that represent a set of parallel planes is of interest. The proposed method is based on the skeletonization technique to create new contours, corresponding to an artificial intermediate slice that models the level where branching occurs. Some experimental results of the application of the proposed method to solve the branching problem on synthetic complex examples and actual medical imaging data are showed. [ABSTRACT FROM AUTHOR]

SUMMARY Objectives: To design an alternative strategy for genotyping cytosine-rich sequences using PCR and nucleotide modification. Methods: The FMR1 gene wild type was modified in the DNA obtained from eight individuals clinically unaffected for Fragile X Syndrome; cytosines were replaced by uracils using sodium bisulfite. Modified DNA was purified and quantified by spectrophotometry. Alternative structures and potential CpG islands of to hybridize with both the modified microsatellite (Primer G) and a modified sequence of CpG islands (Primer M) using the MethPrimer software. Finally, both sequences were amplified by PCR and the amplicons were separated by electrophoresis in silver-stained PAGE 6% gels. Results: The DNA modification was evidenced by spectrophotometry to uracil. We found two potential CpG islands. The amplification with T primers confirmed the "in silico" design developed to engage hairpin structures. The amplification with M primers detected methylation of the first CpG island in the FMR1 gene. Conclusion: We propose an alternative design for amplifying microsatellite sequences that contain methylated and unmethylated cytosine bases. Further studies are required with DNA samples containing expanded microsatellites to validate its molecular diagnostic application. [ABSTRACT FROM AUTHOR]

Copyright of Revista Chapingo Serie Ciencias Forestales is the property of Universidad Autonoma Chapingo and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)