La ciudad: Crecimiento(s) urbano(s) desconfigurados en los contextos de desigualdad y segregación en Lima Metropolitana

This article addresses urban growth in Metropolitan Lima in a context of inequality. It aims to identify the city’s uneven urban growth and the high level of urban fragmentation and segregation that has been predominant over the past decade. It is analyzed from the perspective of urban sociology how a new social, cultural and economic overflow has been produced and reproduced in the city. We maintain that in Metropolitan Lima it has been configured as a segregated and segregated city. Methodologically, a documentary analysis and a review of bibliographic sources are proposed. Finally, by way of conclusions, the need to know and recognize the urban problems of our city is affirmed for a greater efficiency and effectiveness of urban policies.El presente artículo aborda el crecimiento urbano en Lima Metropolitana en un contexto de desigualdad. Tiene por objetivo identificar el crecimiento urbano desconfigurado de la ciudad y el alto nivel de fragmentación y segregación urbana que ha sido predominante durante la última década. Se analiza desde la perspectiva de la sociología urbana cómo se ha producido y reproducido en la ciudad un nuevo desborde social, cultural y económico. Sostenemos que en Lima Metropolitana se ha configurado como una ciudad segregadora y segregada. Metodológicamente se plantea un análisis documental y una revisión de fuentes bibliográficas. Finalmente, a modo de conclusiones, se afirma la necesidad de conocer y reconocer la problemática urbana de nuestra ciudad para un mayor eficiencia y eficacia de las políticas urbanas

Aplicación móvil para la mejora de la memoria semántica de niños con síndrome de down

Como todo trabajo académico estudio es la respuesta a la incógnita: ¿Cuál es el efecto del manejo de aplicaciones móviles en la mejora de la memoria semántica de los niños con síndrome de Down? sobre el cimiento de los diversos estudios literarios de esta temática, aplicados por distintos estudiosos que determinaron diversos problemas y serán elaborados en este trabajo. La tarea principal de la presente fue hallar y determinar el resultado de las aplicaciones móviles en la mejora de la memoria semántica de los infantes con trastorno genético de trisomía del par 21. Para el presente proyecto se tomó como tipo de investigación un diseño preexperimental enfocándonos a un resultado cuantitativo, tomando como referencia a institutos de terapias de rehabilitación y colegios con habilidades especiales con los requisitos necesarios para una evaluación compleja y un porcentaje acertado para la investigación. Se recomienda en caso de querer replicar dicha aplicación móvil para la mejora de la memoria semántica que facilite el desarrollo que ejerce las habilidades de niños capacidades especiales con una mayor facilidad en el progreso de la memoria semántica apoyando la atención por parte de los alumnos, incrementando su capacidad cognitiva, permitiendo mejorar su habilidad de percepción y vincularse con el ambiente que lo rodea

Dinuclear cobalt(III) and mixed valence trinuclear Mn-III-Mn-II-Mn-III complexes with a tripodal bridging pyridylaminophenol ligand

A dinuclear cobalt(II), [Co2(kappa(4)-O,O', N,N'-L)(2)(mu-O,O'-HCOO)](ClO4)center dot(C2H5)(2)O (1) and a linear mixed valence trinuclear manganese, [Mn-3(kappa(4)-O,O', N,N'-L)(2)(mu-CH3O)(2)(mu-O,O'-CH3COO)(2)]center dot 2(C2H5)(2)O (2) complexes with the ligand N-(2-pyridyl-methyl)-N, N-bis-[2'-hydroxy-5'-methyl-benzyl]-amine (H2L) are reported. For both complexes the ligand is present in the deprotonated form. The coordination sphere of the cobalt centres can be described as slightly distorted octahedral with two bridging O-phenoxo, one N-pyridine, one N-amine, one terminal O-phenoxo and one bridging O-formate donor atoms. Interestingly, the bridging formate resulted from the aerial oxidation of methanol. The manganese complex (2) has a linear mixed valence Mn-III-Mn-II-Mn-III, with the Mn-II and Mn-III centres bridged by alkoxo, carboxylate and phenoxo groups. Cyclic voltammetry studies show both metal and ligand centred redox processes consistent with the structure of the complexes. Complex (2) has an S = 3/2 ground state; magnetic susceptibility measurements indicate a weak antiferromagnetic interaction. The best fit of the magnetic susceptibility data as a function of temperature was obtained using a conventional trinuclear linear model [H = -2J(S1S2 + S1S3)] with J = -0.79 cm(-1) and g = 1.99

Genomic characterization of individuals presenting extreme phenotypes of high and low risk to develop tobacco-induced lung cancer

Single nucleotide polymorphisms (SNPs) may modulate individual susceptibility to carcinogens. We designed a genome-wide association study to characterize individuals presenting extreme phenotypes of high and low risk to develop tobacco-induced non-small cell lung cancer (NSCLC), and we validated our results. We hypothesized that this strategy would enrich the frequencies of the alleles that contribute to the observed traits. We genotyped 2.37 million SNPs in 95 extreme phenotype individuals, that is: heavy smokers that either developed NSCLC at an early age (extreme cases); or did not present NSCLC at an advanced age (extreme controls), selected from a discovery set (n = 3631). We validated significant SNPs in 133 additional subjects with extreme phenotypes selected from databases including >39,000 individuals. Two SNPs were validated: rs12660420 (pcombined  = 5.66 × 10-5 ; ORcombined  = 2.80), mapping to a noncoding transcript exon of PDE10A; and rs6835978 (pcombined  = 1.02 × 10-4 ; ORcombined  = 2.57), an intronic variant in ATP10D. We assessed the relevance of both proteins in early-stage NSCLC. PDE10A and ATP10DmRNA expressions correlated with survival in 821 stage I-II NSCLC patients (p = 0.01 and p < 0.0001). PDE10A protein expression correlated with survival in 149 patients with stage I-II NSCLC (p = 0.002). In conclusion, we validated two variants associated with extreme phenotypes of high and low risk of developing tobacco-induced NSCLC. Our findings may allow to identify individuals presenting high and low risk to develop tobacco-induced NSCLC and to characterize molecular mechanisms of carcinogenesis and resistance to develop NSCLC.This work was supported by the Spanish Society of Medical Oncology; Fundación SEOM and Fundación Salud 2000; and Government of Navarra.S

Genomic characterization of individuals presenting extreme phenotypes of high and low risk to develop tobacco-induced lung cancer

Single nucleotide polymorphisms (SNPs) may modulate individual susceptibility to carcinogens. We designed a genome-wide association study to characterize individuals presenting extreme phenotypes of high and low risk to develop tobacco-induced non-small cell lung cancer (NSCLC), and we validated our results. We hypothesized that this strategy would enrich the frequencies of the alleles that contribute to the observed traits. We genotyped 2.37 million SNPs in 95 extreme phenotype individuals, that is: heavy smokers that either developed NSCLC at an early age (extreme cases); or did not present NSCLC at an advanced age (extreme controls), selected from a discovery set (n=3631). We validated significant SNPs in 133 additional subjects with extreme phenotypes selected from databases including >39,000 individuals. Two SNPs were validated: rs12660420 (p(combined)=5.66x10(-5); ORcombined=2.80), mapping to a noncoding transcript exon of PDE10A; and rs6835978 (p(combined)=1.02x10(-4); ORcombined=2.57), an intronic variant in ATP10D. We assessed the relevance of both proteins in early-stage NSCLC. PDE10A and ATP10D mRNA expressions correlated with survival in 821 stage I-II NSCLC patients (p=0.01 and p<0.0001). PDE10A protein expression correlated with survival in 149 patients with stage I-II NSCLC (p=0.002). In conclusion, we validated two variants associated with extreme phenotypes of high and low risk of developing tobacco-induced NSCLC. Our findings may allow to identify individuals presenting high and low risk to develop tobacco-induced NSCLC and to characterize molecular mechanisms of carcinogenesis and resistance to develop NSCLC

De novo mutations of KIAA2022 in females cause intellectual disability and intractable epilepsy

Background Mutations in the KIAA2022 gene have been reported in male patients with X-linked intellectual disability, and related female carriers were unaffected. Here, we report 14 female patients who carry a heterozygous de novo KIAA2022 mutation and share a phenotype characterised by intellectual disability and epilepsy. Methods Reported females were selected for genetic testing because of substantial developmental problems and/or epilepsy. X-inactivation and expression studies were performed when possible. Results All mutations were predicted to result in a frameshift or premature stop. 12 out of 14 patients had intractable epilepsy with myoclonic and/or absence seizures, and generalised in 11. Thirteen patients had mild to severe intellectual disability. This female phenotype partially overlaps with the reported male phenotype which consists of more severe intellectual disability, microcephaly, growth retardation, facial dysmorphisms and, less frequently, epilepsy. One female patient showed completely skewed X-inactivation, complete absence of RNA expression in blood and a phenotype similar to male patients. In the six other tested patients, X-inactivation was random, confirmed by a non-significant twofold to threefold decrease of RNA expression in blood, consistent with the expected mosaicism between cells expressing mutant or normal KIAA2022 alleles. Conclusions Heterozygous loss of KIAA2022 expression is a cause of intellectual disability in females. Compared with its hemizygous male counterpart, the heterozygous female disease has less severe intellectual disability, but is more often associated with a severe and intractable myoclonic epilepsy

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead