Universidad del Desarrollo

About: Universidad del Desarrollo is a education organization based out in Santiago, Chile. It is known for research contribution in the topics: Population & Entrepreneurship. The organization has 2695 authors who have published 3578 publications receiving 52302 citations.

Exclusion Criteria for Intravenous Thrombolysis in Stroke Mimics: An Observational Study

Abstract: Background Stroke mimics (SMs) are frequent in emergency departments (EDs), but are treated infrequently with intravenous recombinant tissue plasminogen activator (rt-PA) thrombolysis. We aimed at identifying the factors that lead to the exclusion of SMs from thrombolytic therapy. Methods Consecutive patients presenting to the ED between December 2004 and March 2011 with symptoms that suggested acute ischemic stroke were included. Results Eight hundred forty-two patients were included in this study; 113 (13.4%) were considered SMs; these patients were younger ( P = .01), more frequently diabetic ( P = .001), arrived later to the ED ( P = .03), had lower National Institutes of Health Stroke Scale scores ( P P = .002). The most common causes of cases of SM were toxic metabolic disorders (n = 34 [30.1%]) and seizures (n = 22 [19.5%]). The most frequent cause of consultation was aphasia (n = 43 [37.6%]). SM patients had a total of 152 contraindications for rt-PA, with 34 (30%) patients having >1 contraindication. The most frequent of these were being beyond the therapeutic window for thrombolysis (n = 96) and having deficits not measurable by the National Institutes of Health Stroke Scale or very mild symptoms before the start of rt-PA (n = 37). Twenty-four (21.2%) patients had both contraindications simultaneously. Two patients (1.76%) in the SM group were candidates for rt-PA but did not receive this treatment because they or their family rejected it. Of 729 stroke patients, 87 (11.9%) did receive rt-PA. Conclusions SM patients frequently had exclusion criteria for systemic thrombolysis, the most frequent being presenting beyond the established thrombolytic window.

Deletion of liaR Reverses Daptomycin Resistance in Enterococcus faecium Independent of the Genetic Background

Abstract: We have shown previously that changes in LiaFSR, a three-component regulatory system predicted to orchestrate the cell membrane stress response, are important mediators of daptomycin (DAP) resistance in enterococci. Indeed, deletion of the gene encoding the response regulator LiaR in a clinical strain of Enterococcus faecalis reversed DAP resistance (DAP-R) and produced a strain hypersusceptible to antimicrobial peptides. Since LiaFSR is conserved in Enterococcus faecium, we investigated the role of LiaR in a variety of clinical E. faecium strains representing the most common DAP-R genetic backgrounds. Deletion of liaR in DAP-R E. faecium R446F (DAP MIC of 16 μg/ml) and R497F (MIC of 24 μg/ml; harboring changes in LiaRS) strains fully reversed resistance (DAP MICs decreasing to 0.25 and 0.094 μg/ml, respectively). Moreover, DAP at concentrations of 13 μg/ml (achieved with human doses of 12 mg/kg body weight) retained bactericidal activity against the mutants. Furthermore, the liaR deletion derivatives of these two DAP-R strains exhibited increased binding of boron-dipyrromethene difluoride (BODIPY)-daptomycin, suggesting that high-level DAP-R mediated by LiaR in E. faecium involves repulsion of the calcium-DAP complex from the cell surface. In DAP-tolerant strains HOU503F and HOU515F (DAP MICs within the susceptible range but bacteria not killed by DAP concentrations of 5× the MIC), deletion of liaR not only markedly decreased the DAP MICs (0.064 and 0.047 μg/ml, respectively) but also restored the bactericidal activity of DAP at concentrations as low as 4 μg/ml (achieved with human doses of 4 mg/kg). Our results suggest that LiaR plays a relevant role in the enterococcal cell membrane adaptive response to antimicrobial peptides independent of the genetic background and emerges as an attractive target to restore the activity of DAP against multidrug-resistant strains.

Factores de resiliencia asociados al rendimiento académico en estudiantes de contextos de alta vulnerabilidad social

Abstract: Resumen es: La presente investigacion analiza la relacion entre factores de resiliencia y rendimiento academico en alumnos adolescentes de establecimientos educativo...

Genetic variants in FGFR2 and MAP3K1 are associated with the risk of familial and early-onset breast cancer in a South-American population

Abstract: Genome-Wide Association Studies have identified several loci associated with breast cancer (BC) in populations of different ethnic origins. One of the strongest associations was found in the FGFR2 gene, and MAP3K1 has been proposed as a low-penetrance BC risk factor. In this study, we evaluated the associations among FGFR2 SNPs rs2981582, rs2420946, and rs1219648; and MAP3K1 rs889312, with BC risk in 351 BRCA1/2-negative Chilean BC cases and 802 controls. All the SNPs studied were significantly associated with increased BC risk in familial BC and in non-familial early-onset BC, in a dose-dependent manner. Subjects with 3 risk alleles were at a significantly increased risk of BC compared with subjects with 0-2 risk alleles, in both familial BC and early-onset non-familial BC (OR = 1.47, 95 % CI 1.04-2.07, P = 0.026 and OR = 2.04 95 % CI 1.32-3.24, P < 0.001, respectively). In the haplotype analysis, the FGFR2 rs2981582 T / rs2420946 T / rs1219648 G haplotype (ht2) was associated with a significantly increased BC risk compared with the rs2981582 C / rs2420946 C / rs1219648 A haplotype in familial BC and in non-familial early-onset BC (OR = 1.32, 95 % CI 1.06-1.65, P = 0.012; OR = 1.46, 95 % CI 1.11-1.91, P = 0.004, respectively). When the FGFR2 ht2 and MAP3K1 rs889312 were evaluated as risk alleles, the risk of BC increased in a dose-dependent manner as the number of risk alleles increased (P trend <0.0001), indicating an additive effect. Nevertheless, there is no evidence of an interaction between FGFR2 ht2 and the MAP3K1 rs889312 C allele. These findings suggest that genetic variants in the FGFR2 and MAP3K1 genes may contribute to genetic susceptibility to BC.