Interacción entre cementos de diferente composición y aditivos superplastificantes

The slump behavior of ordinary Portland-, pozzolanic (red brick powder)-, sulfate resistant-, and limestone cement pastes caused by ≤ 1% additions of polycondensates and polycarboxylates superplasticizers are monitored for up to 90 minutes. With the plolycondensates, Portland- and pozzolanic cements gain fluidity at higher dosages than sulfate resistant and limestone cements. Limestone cement shows the best slump retention. The aluminate and sulfate phases play a major role in the fluidity. With the polycarboxylates, all cements gain fluidity with dosages of ≤ 0.3%. A polycarboxylate with no resonance of methyl methylene proton in the main chain identified in the NMR spectra creates good slump retention. This is explained by a low mobility of the structure and the predominance of the steric effect. The polycarboxylate shows also strong ether bands relative to the ester groups in the IR spectra and a low polydispersity observed in the elution of few low molecular weight species in the HPLC chromatogram.Se ha estudiado el efecto fluidificante (hasta 90 minutos) ejercido por la incorporación de entre 0-1% de aditivos policondensados y policarboxilatos en pastas de cemento Portland, puzolánico, resistente a sulfatos y con adición de caliza. Con la incorporación de los aditivos policondensados, se produjo un incremento de la fluidez de los cementos Portland y puzolánico a mayores dosificaciones que las necesarias en los cementos resistente a sulfatos y con adición de caliza. Éste último presentó la mejor retención de la fluidez. Las fases aluminatos y sulfatos juegan un importante papel en la fluidez inducida. Todos los cementos incrementaron su fluidez con la incorporación de aditivos policarboxilatos a dosificaciones menores del 0,3%. El policarboxilato que no presenta en los espectros de RMN, resonancia asignada al protón de los grupos metil metileno, presenta buena retención de la fluidez. Esto es debido a la baja flexibilidad de la estructura y predominancia del efecto estérico. Este aditivo presenta también, mayor relación de grupos eter frente a grupos ester en los espectros IR, asi como una baja polidispersidad observada en la elución de especies de bajo peso molecular a través de HPLC

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe