Los programas de mediación entre iguales: una herramienta eficaz para la convivencia escolar

A pesar de las ventajas de los sistemas de mediación entre iguales, todavía son escasos los estudios que incorporan una evaluación científica del impacto de estos programas. Por ello, el objetivo de este estudio era el de analizar el impacto de los programas de mediación entre iguales en Educación Secundaria, a través de los roles que adoptaban los menores ante los conflictos, así como de sus actitudes províctima. Para lograr este objetivo, se compararon dos centros públicos de Educación Secundaria, de similares características, uno de ellos con programa de mediación entre iguales, y el otro, sin programa de mediación. En ambos centros, se administró la Escala de roles “Adivina quién” (Salmivalli et al., 1996; adaptada por Sutton y Smith, 1999), a 323 alumnos de 12-15 años, tanto en tiempo 1 (situación inicial), como en tiempo 2 (tras la aplicación del programa). Los resultados muestran, en el centro sin programa de mediación escolar, fundamentalmente un incremento de las actitudes províctima, lo cual apunta hacia una mejora explícita en el centro con mediación.Although the advantages of peer mediation systems are outstanding, few studies have included a longitudinal design and a scientific measure of the impact of these programs. In this sense, the objective of this study was to analyse the impact of peer mediation programs in high school education, throughout the roles adopted in the conflict, and the attitudes pro-victim. In order to attain this goal, two public high schools, with similar characteristics, were compared: one developing a peer mediation program, and one not developing it. The Role Scale Nominations from Salmivalli et al. (1996), was administered to 323 students from 12-15 years old, in time 1 (baseline), and time 2 (after program development). Results showed mainly the increase of the attitudes pro-victim in the school with mediation program, indicating a clear improvement due to this type of programs.Ministerio de Educación EDU2010-21791Fundació Caixa P1.1B2010-16Castelló Bancaixa P1.1B2010-1

Bursitis del psoas-ilíaco

La bolsa serosa del psoas-ilíaco es una estructura anatómica bien definida, habitualmente presente en el adulto. La comunicación entre dicha bolsa y la articulación de la cadera se asocia frecuentemente a la coxartria. Presentamos un caso de agrandamiento de la bolsa serosa del psoas ilíaco en una paciente de 69 años. El diagnóstico de sospecha se estableció por la presencia de una masa inguinal y dolor de cadera. La ecografía y la T.A.C. confirmaron el diagnóstico. Tras la punción de la bolsa y la instilación de corticoides hemos obtenido la remisión de los síntomas.The iliopsoas bursa is a well-defined anatomic structure rarely absent in adults. Communication existing between the iliopsoas bursa and the hip joint is frequently associated with preexisting hip arthrosis. We present a case of iliopsoas bursa enlargement in a 69-yearold woman. The diagnosis was suspected by the presence of inguinal mass and hip pain. Echography, and later computed tomography confirmed it. The patient was successfully treated with aspiration of cyst content and steroid instillation

The compositional and evolutionary logic of metabolism

Metabolism displays striking and robust regularities in the forms of modularity and hierarchy, whose composition may be compactly described. This renders metabolic architecture comprehensible as a system, and suggests the order in which layers of that system emerged. Metabolism also serves as the foundation in other hierarchies, at least up to cellular integration including bioenergetics and molecular replication, and trophic ecology. The recapitulation of patterns first seen in metabolism, in these higher levels, suggests metabolism as a source of causation or constraint on many forms of organization in the biosphere. We identify as modules widely reused subsets of chemicals, reactions, or functions, each with a conserved internal structure. At the small molecule substrate level, module boundaries are generally associated with the most complex reaction mechanisms and the most conserved enzymes. Cofactors form a structurally and functionally distinctive control layer over the small-molecule substrate. Complex cofactors are often used at module boundaries of the substrate level, while simpler ones participate in widely used reactions. Cofactor functions thus act as "keys" that incorporate classes of organic reactions within biochemistry. The same modules that organize the compositional diversity of metabolism are argued to have governed long-term evolution. Early evolution of core metabolism, especially carbon-fixation, appears to have required few innovations among a small number of conserved modules, to produce adaptations to simple biogeochemical changes of environment. We demonstrate these features of metabolism at several levels of hierarchy, beginning with the small-molecule substrate and network architecture, continuing with cofactors and key conserved reactions, and culminating in the aggregation of multiple diverse physical and biochemical processes in cells.Comment: 56 pages, 28 figure

Phenotypic Variation and Bistable Switching in Bacteria

Microbial research generally focuses on clonal populations. However, bacterial cells with identical genotypes frequently display different phenotypes under identical conditions. This microbial cell individuality is receiving increasing attention in the literature because of its impact on cellular differentiation, survival under selective conditions, and the interaction of pathogens with their hosts. It is becoming clear that stochasticity in gene expression in conjunction with the architecture of the gene network that underlies the cellular processes can generate phenotypic variation. An important regulatory mechanism is the so-called positive feedback, in which a system reinforces its own response, for instance by stimulating the production of an activator. Bistability is an interesting and relevant phenomenon, in which two distinct subpopulations of cells showing discrete levels of gene expression coexist in a single culture. In this chapter, we address techniques and approaches used to establish phenotypic variation, and relate three well-characterized examples of bistability to the molecular mechanisms that govern these processes, with a focus on positive feedback.

Inhibition of Competence Development, Horizontal Gene Transfer and Virulence in Streptococcus pneumoniae by a Modified Competence Stimulating Peptide

Competence stimulating peptide (CSP) is a 17-amino acid peptide pheromone secreted by Streptococcus pneumoniae. Upon binding of CSP to its membrane-associated receptor kinase ComD, a cascade of signaling events is initiated, leading to activation of the competence regulon by the response regulator ComE. Genes encoding proteins that are involved in DNA uptake and transformation, as well as virulence, are upregulated. Previous studies have shown that disruption of key components in the competence regulon inhibits DNA transformation and attenuates virulence. Thus, synthetic analogues that competitively inhibit CSPs may serve as attractive drugs to control pneumococcal infection and to reduce horizontal gene transfer during infection. We performed amino acid substitutions on conserved amino acid residues of CSP1 in an effort to disable DNA transformation and to attenuate the virulence of S. pneumoniae. One of the mutated peptides, CSP1-E1A, inhibited development of competence in DNA transformation by outcompeting CSP1 in time and concentration-dependent manners. CSP1-E1A reduced the expression of pneumococcal virulence factors choline binding protein D (CbpD) and autolysin A (LytA) in vitro, and significantly reduced mouse mortality after lung infection. Furthermore, CSP1-E1A attenuated the acquisition of an antibiotic resistance gene and a capsule gene in vivo. Finally, we demonstrated that the strategy of using a peptide inhibitor is applicable to other CSP subtype, including CSP2. CSP1-E1A and CSP2-E1A were able to cross inhibit the induction of competence and DNA transformation in pneumococcal strains with incompatible ComD subtypes. These results demonstrate the applicability of generating competitive analogues of CSPs as drugs to control horizontal transfer of antibiotic resistance and virulence genes, and to attenuate virulence during infection by S. pneumoniae

A Novel Mechanism of Programmed Cell Death in Bacteria by Toxin–Antitoxin Systems Corrupts Peptidoglycan Synthesis

Most genomes of bacteria contain toxin–antitoxin (TA) systems. These gene systems encode a toxic protein and its cognate antitoxin. Upon antitoxin degradation, the toxin induces cell stasis or death. TA systems have been linked with numerous functions, including growth modulation, genome maintenance, and stress response. Members of the epsilon/zeta TA family are found throughout the genomes of pathogenic bacteria and were shown not only to stabilize resistance plasmids but also to promote virulence. The broad distribution of epsilon/zeta systems implies that zeta toxins utilize a ubiquitous bacteriotoxic mechanism. However, whereas all other TA families known to date poison macromolecules involved in translation or replication, the target of zeta toxins remained inscrutable. We used in vivo techniques such as microscropy and permeability assays to show that pneumococcal zeta toxin PezT impairs cell wall synthesis and triggers autolysis in Escherichia coli. Subsequently, we demonstrated in vitro that zeta toxins in general phosphorylate the ubiquitous peptidoglycan precursor uridine diphosphate-N-acetylglucosamine (UNAG) and that this activity is counteracted by binding of antitoxin. After identification of the product we verified the kinase activity in vivo by analyzing metabolite extracts of cells poisoned by PezT using high pressure liquid chromatograpy (HPLC). We further show that phosphorylated UNAG inhibitis MurA, the enzyme catalyzing the initial step in bacterial peptidoglycan biosynthesis. Additionally, we provide what is to our knowledge the first crystal structure of a zeta toxin bound to its substrate. We show that zeta toxins are novel kinases that poison bacteria through global inhibition of peptidoglycan synthesis. This provides a fundamental understanding of how epsilon/zeta TA systems stabilize mobile genetic elements. Additionally, our results imply a mechanism that connects activity of zeta toxin PezT to virulence of pneumococcal infections. Finally, we discuss how phosphorylated UNAG likely poisons additional pathways of bacterial cell wall synthesis, making it an attractive lead compound for development of new antibiotics