Assessment of pH Value and Release of Calcium Ions in Calcium Silicate Cements: An In Vitro Comparative Study.

The goal of this study was to evaluate the pH and the release of calcium from four calcium-silicate-based cements. METHODS: Four materials were tested (ProClinic MTA; Angelus MTA; ProRoot MTA; Biodentine). The palatal canal root of acrylic upper molars was filled with each cement. Afterwards, they were set in phosphate-buffered saline. Measurements were taken by atomic adsorption spectroscopy (AAS) at 3, 24, 72, 168, 336, 672, and 1008 h. The pH was measured at the same timepoints. Kruskal-Wallis tests were carried out in each period, as the Kolmogorov-Smirnov and Shapiro-Wilk tests showed no parametric results. RESULTS: Significant differences (p < 0.05) in calcium release were found at the 3-, 24-, and 72-hour evaluations. All of the analyzed groups presented a release of calcium ions up to 168 h, and the general tendency was to increase up to 672 h, with a maximum release of 25.45 mg/g in the ProRoot group. We could only observe significant differences (p < 0.05) in pH value over 168 h between the Biodentine (7.93) and Angelus MTA (7.31) groups. CONCLUSIONS: There were significant differences (p < 0.05) in calcium release. Nevertheless, no significant differences (p > 0.05) in the pH values were found at the studied timepoints, except for the values at 168 h.

Improving Matching Between Recipient and Donor in Liver Transplantation: Are Scores Able to Predict Long-term Survival?

BACKGROUND: The primary goal was to calculate the value of delta Model for End-Stage Liver Disease (D-MELD) and Balance of Risk (BAR) scores in patients who underwent liver transplant. The secondary objective was to evaluate D-MELD and BAR scores' ability to predict patient and graft survival. METHODS: We retrospectively evaluated 336 patients who underwent liver transplant in a tertiary medical center between January 2010 and December 2020. The D-MELD and the BAR scores were evaluated through a receiver operating characteristic curve with the calculation of area under the curve (AUC) to evaluate the predictive score power for 3-month, 6-month, 1-year, and 5-year patient and graft survivals. RESULTS: The AUCs of D-MELD score in predicting 5-year patient and graft survival were 0.506 (95% CI, 0.43-0.57) and 0.49 (95% CI, 0.42-0.56), respectively. The AUCs of BAR score in predicting 5-year patient and graft survival were 0.50 (95% CI, 0.33-0.66) and 0.49 (95% CI, 0.30-0.67), respectively. CONCLUSIONS: We could not confirm the ability to predict long-term survival by using D-MELD and BAR scores in our sample; however, there is a statistically significant trend in receiver operating characteristic curves of 5-year patient and graft survivals. We encourage the use of new scoring systems with a greater external validation to improve allograft allocation.

Diagnostic utility of HFE variants in Spanish patients: association with HLA alleles and role in susceptibility to acute lymphoblastic leukemia.

Two single nucleotide polymorphisms (SNPs) in the Human Hemochromatosis (HFE) gene, C282Y and H63D, are the major variants associated to altered iron status and it is well known that these mutations are in linkage disequilibrium with certain Human Leukocyte Antigen (HLA)-A alleles. In addition, the C282Y SNP has been previously suggested to confer susceptibility to acute lymphoblastic leukemia (ALL). We have aimed to assess the diagnosis utility of these polymorphisms in a population of Spanish subjects with suspicion of hereditary iron overload and to evaluate the effect of their associations with HLA-A alleles on the susceptibility to ALL. Both the 63DD [OR=4.31 (1.7-11.2)] and 282YY (p for trend=0.02) genotypes were more frequently found among subjects with suspicion of iron overload than among controls. 282YY carriers displayed significantly higher transferrin saturation index (TSI) values (p<0.001) as well as serum iron (p=0.01) and ferritin (p=0.01) levels. In addition, transferrin levels were lower in these subjects (p=0.01). Likewise, patients who were carriers of the compound heterozygous diplotype (282CY/63HD) showed significantly higher TSI and serum iron and ferritin concentrations. The H63D SNP did not significantly affect the analytical parameters measured. All 282YY carriers and 69.2% of compound heterozygotes showed an altered biochemical index. The frequencies of the HFE SNPs in ALL pediatric patients were lower than those found in controls, whereas the HLA-A*24 allele was significantly overrepresented in the patients group [OR=3.76 (1.9-7.3)]. No HFE-HLA-A associations were found to modulate the ALL risk. These results suggest that it may be useful to test for both HFE H63D and C282Y polymorphisms in patients with iron overload, as opposed to just genotyping for the C282Y SNP, which is customary in some healthcare centers. These HFE variants and their associations with HLA-A alleles were not observed to be relevant for the susceptibility to ALL in our population.

Asociación de polimorfismos en el gen FTO con la obesidad mórbida en la población extremeña / Association of FTO gene polymorphisms and morbid obesity in the population of Extremadura (Spain)

ObjetivoSeleccionar individuos cuya obesidad mórbida (OM) se pueda atribuir preferentemente al perfil genético individual. Tras descartar pacientes con posibles síndromes monogénicos y otras enfermedades con obesidad asociada, evaluar la asociación de la variabilidad del gen FTO (asociado con la masa grasa y la obesidad), sobre la base de los polimorfismos de un solo nucleótido (SNP) con rs1861868 y rs9939609, con la predisposición heredada a padecer OM.Pacientes y métodosTras evaluar a 270 pacientes con OM instaurada antes de los 14 años, seleccionamos a 194 por su fenotipo y la historia familiar referida; se incluyó a 289 individuos controles. Se genotiparon los cambios en el SNP rs1861868 y rs9939609 del gen FTO, y comparamos sus frecuencias genotípicas y haplotípicas en ambos grupos poblacionales.ResultadosSe confirmó la asociación del alelo A del SNP rs9939609 con la obesidad grave instaurada en la infancia en la población española. Los individuos portadores del haplotipo rs1861868 G/rs9939609 A del gen FTO mostraron un incremento del riesgo (odds ratio de 3,03; intervalo de confianza del 95%: 1,74–5,27) a padecer obesidad mórbida en nuestra población.ConclusiónAnalizar las bases genéticas de la obesidad precisa una rigurosa selección de los casos. La asociación del SNP rs9939609 con la obesidad, ampliamente descrita en distintas poblaciones, se confirma en la población española. Identificamos el primer haplotipo de riesgo al analizar el SNP rs1861868 del bloque haplotípico contiguo al que contiene el primero. Es preciso estudiar en profundidad la variabilidad interindividual del gen FTO para identificar la causa de su capacidad deletérea a la enfermedad (AU)

ObjectiveTo select individuals whose morbid obesity can be attributed mainly to their individual genetic profile. After excluding patients with potential monogenic syndromes or diseases associated with obesity, we evaluated the association of the single nucleotide polymorphisms (SNPs) rs1861868 and rs9939609 of the fat-mass and obesity-associated FTO gene with an inherited predisposition to morbid obesity.Patients and methodsWe evaluated 270 patients with morbid obesity and onset before the age of 14 years and selected 194 due to their phenotypes and family history; 289 control individuals were included. The rs1861868 and rs9939609 variants, located in the FTO gene, were genotyped. Genotype and haplotype frequencies were compared between cases and controls.ResultsThe A allele of rs9939609 was associated with severe obesity starting in childhood among the Spanish population. The rs1861868 G/rs9939609 A haplotype of the FTO gene was also significantly associated with severe obesity in our population, with an odds ratio of 3.03 (95% confidence interval, 1.74–5.27).ConclusionAnalysis of the genetic basis of obesity requires rigorous selection of cases. In this study, the association of the rs9939609 SNP with obesity widely described in distinct populations was confirmed among overweight Spanish children. Genotyping rs1861868 allowed us to identify the first risk haplotype in the FTO gene, which is located in the adjacent haplotype block containing rs9939609. In-depth study of the variability of the FTO gene is essential to define its deleterious capacity (AU)

[Association of FTO gene polymorphisms and morbid obesity in the population of Extremadura (Spain)]. / Asociación de polimorfismos en el gen FTO con la obesidad mórbida en la población extremeña.

OBJECTIVE: To select individuals whose morbid obesity can be attributed mainly to their individual genetic profile. After excluding patients with potential monogenic syndromes or diseases associated with obesity, we evaluated the association of the single nucleotide polymorphisms (SNPs) rs1861868 and rs9939609 of the fat-mass and obesity-associated FTO gene with an inherited predisposition to morbid obesity. PATIENTS AND METHODS: We evaluated 270 patients with morbid obesity and onset before the age of 14 years and selected 194 due to their phenotypes and family history; 289 control individuals were included. The rs1861868 and rs9939609 variants, located in the FTO gene, were genotyped. Genotype and haplotype frequencies were compared between cases and controls. RESULTS: The A allele of rs9939609 was associated with severe obesity starting in childhood among the Spanish population. The rs1861868 G/rs9939609 A haplotype of the FTO gene was also significantly associated with severe obesity in our population, with an odds ratio of 3.03 (95% confidence interval, 1.74-5.27). CONCLUSION: Analysis of the genetic basis of obesity requires rigorous selection of cases. In this study, the association of the rs9939609 SNP with obesity widely described in distinct populations was confirmed among overweight Spanish children. Genotyping rs1861868 allowed us to identify the first risk haplotype in the FTO gene, which is located in the adjacent haplotype block containing rs9939609. In-depth study of the variability of the FTO gene is essential to define its deleterious capacity.

Hemosuccus pancreaticus causado por un seudoaneurisma de la arteria esplénica / Haemosuccus pancreaticus caused by a splenic artery pseudoaneurysm

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Effect of pretreatment with interleukin-1 beta on inflammatory infiltrates and tissue damage after experimental endotoxic challenge.

OBJECTIVE: To evaluate the effect of treatment with murine recombinant interleukin-1 beta on inflammatory infiltrate and tissue damage after experimental endotoxic challenge. DESIGN: Randomized, controlled study. SETTING: Experimental Unit, Virgen de las Nieves University Hospital. SUBJECTS: Seventy-two female CBA/H mice, 20-21 g, supplied by the animal center of the Experimental Unit. INTERVENTION: The mice were randomized into three groups of 24. Group 1 (sham) received two intraperitoneal doses of 0.1 mL of phosphate-buffered saline; group 2 (lipopolysaccharide) was injected with 125 mg/kg lipopolysaccharide (Escherichia coli, intraperitoneally) 24 hrs after 0.1 mL of phosphate-buffered saline; group 3 was pretreated with 80 ng of recombinant interleukin-1 beta per mouse (intraperitoneally) 24 hrs before the endotoxic challenge. MEASUREMENTS AND MAIN RESULTS: At 1, 2, 4, and 24 hrs after the endotoxic challenge, we studied inflammatory infiltrate and tissue damage in lung, liver, and intestine by determining myeloperoxidase and malondialdehyde tissue concentrations. When we compared the pretreated group with the lipopolysaccharide group, myeloperoxidase concentrations decreased significantly in lung (p <.001) and liver (p <.001) at all study times, and in intestine (p <.001) at 2, 4, and 24 hrs; malondialdehyde concentrations significantly decreased in lung at 1 (p <.05), 2 (p <.01), and 24 (p <.001) hrs, in liver at 2 (p <.001), 4 (p <.01), and 24 (p <.001) hrs, and in intestine at 1 (p <.001), 2, 4 (p <.05), and 24 (p <.001) hrs. CONCLUSION: Pretreatment with recombinant interleukin-1 beta significantly reduces inflammatory infiltrate and tissue damage in mouse lung, liver, and intestine after an experimental endotoxic challenge.