Facebook como herramienta educativa para incentivar el debate sobre noticias de interés toxicológico

Memoria ID-214. Ayudas de la Universidad de Salamanca para la innovación docente, curso 2019-2020

Facebook como herramienta educativa para incentivar el debate sobre noticias de interés toxicológico

Memoria ID-214. Ayudas de la Universidad de Salamanca para la innovación docente, curso 2019-2020

POÉTICAS DECOLONIAIS: : RESSIGNIFICAÇÃO RACIAL NEGRA EM MARY GRUESO ROMERO E LUCIENE NASCIMENTO

A poesia produzida por mulheres afro-latino-americanas é um dos mais poderosos caminhos de resistência cultural a serem referenciados na diáspora negra da América Latina e Caribe. Neste artigo, analisa-se como a colombiana Mary Grueso Romero e a brasileira Luciene Nascimento, a partir da voz, da memória e do corpo feminino negro, conseguem criar percursos de insurgência capazes de ressignificar, poeticamente, a identidade racial e promover uma virada decolonial frente aos discursos hegemônicos

Influence of 2% Chlorhexidine on the Bond Strength of Three Adhesive Systems on Primary Molars: An In Vitro Study

The hydrolysis of the collagen matrix by metalloproteinases (MMPs) is one of the paradigms that currently arouses most interest due to its close relationship with a decrease in bond strength (BS) and consequent restoration failure. Chlorhexidine 2% has demonstrated its ability to inhibit MMPs’ activity in the permanent dentition, improving the duration of resin–dentine, but there are few studies on deciduous dentition and its possible repercussions. Aim: To determine the influence of 2% chlorhexidine digluconate (CHX) as a dentine pretreatment on the BS of three adhesive systems on primary molars. Methods: 128 primary extracted molars were assigned to eight groups at random. BS in vitro was recorded by micropush-out test, and analyzed by two-way ANOVA. Results: BS values oscillated from 15.01 MPa to 20.41 MPa. There was no statistically relevant variation between the BS total mean of those adhesive groups that had received CHX pretreatment versus those that did not. Adper Prompt L-Pop was the self-etching adhesive with the best BS. Adper Scotchbond 1XT was the total-etch adhesive with the best BS values. Conclusions: Application of 2% chlorhexidine for 60 s as dentine pretreatment did not affect the immediate BS of several adhesive systems used in primary dentition

Acquired predisposition to renal damage associated to tobacco consumption

A relation between tobacco and renal damage has been described during the last years. Referring to early diagnosis of renal disease, our group has developed the acquired predisposition concept, which can be applied to the smoking patient context. So, our hypothesis is that tobacco may cause predisposition to acute kidney injury (AKI), which means smokers may suffer AKI after being exposed to any nephrotoxin, including under-toxicity-level doses. Our aim was to study the relationship between the predisposition biomarkers 1 (BM1), 2 (BM2) and 3 (BM3) (characterized in our laboratory) and tobacco consumption./nUrinary samples were taken from smokers and non-smokers volunteers with no renal damage nor exposure to risk factors of renal disease. The plasma creatinine of the patients was obtained from their medical history. The cotinine levels, which inform of the grade of smoking, were measured by ELISA. The urinary creatinine, used to correct urinary concentrations of biomarkers, was measured with a commercial kit based on Jaffé reaction, and the urinary biomarkers levels were measured by Western blot./nOnly BM3 showed greater excretion in smoking patients than in non-smokers. However, that excretion is not related to cotinine levels. In any case, BM3 could be a good clinical biomarker of AKI predisposition which would help to prevent renal damage in smokers.En los últimos años se ha visto una relación entre el tabaquismo y el daño renal. En cuanto al diagnóstico temprano del daño renal, nuestro grupo ha desarrollado el concepto de predisposición, aplicable al contexto de pacientes fumadores. Así, nuestra hipótesis es que el tabaco podría causar predisposición a sufrir daño renal agudo (DRA), lo que supondría que los fumadores podrían padecer DRA tras ser expuestos a alguna nefrotoxina, incluyendo dosis inferiores al límite tolerable. Nuestro objetivo es estudiar la relación entre los biomarcadores caracterizados en nuestro laboratorio: 1, 2 y 3 (BM1, BM2 y BM3) y el consumo de tabaco./nSe tomaron muestras de orina de pacientes fumadores y no fumadores, sin daño renal ni exposición a factores de riesgo de este. Se midieron la cotinina (ELISA), la creatininuria (kit comercial) y los biomarcadores (western blot). La creatinina plasmática se obtuvo del historial clínico de los pacientes./nSolo se vio una mayor excreción de BM3 en fumadores con respecto a no fumadores, aunque no se obtuvo una correlación con los niveles de cotinina (metabolito de nicotina que informa del grado de tabaquismo). A pesar de ello, BM3 podría suponer un buen biomarcador clínico para detectar la predisposición al DRA, lo que ayudaría a prevenir el daño renal en pacientes fumadores./n

Antibiotics shaping bacterial genome: deletion of an IS91 flanked virulence determinant upon exposure to suinhibitory antibiotic concentrations

The nucleoid-associated proteins Hha and YdgT repress the expression of the toxin α-hemolysin. An Escherichia coli mutant lacking these proteins overexpresses the toxin α-hemolysin encoded in the multicopy recombinant plasmid pANN202-312R. Unexpectedly, we could observe that this mutant generated clones that no further produced hemolysin (Hly-). Generation of Hly- clones was dependent upon the presence in the culture medium of the antibiotic kanamycin (km), a marker of the hha allele (hha::Tn5). Detailed analysis of different Hly- clones evidenced that recombination between partial IS91 sequences that flank the hly operon had occurred. A fluctuation test evidenced that the presence of km in the culture medium was underlying the generation of these clones. A decrease of the km concentration from 25 mg/l to 12.5 mg/l abolished the appearance of Hly- derivatives. We considered as a working hypothesis that, when producing high levels of the toxin (combination of the hha ydgT mutations with the presence of the multicopy hemolytic plasmid pANN202-312R), the concentration of km of 25 mg/l resulted subinhibitory and stimulated the recombination between adjacent IS91 flanking sequences. To further test this hypothesis, we analyzed the effect of subinhibitory km concentrations in the wild type E. coli strain MG1655 harboring the parental low copy number plasmid pHly152. At a km concentration of 5 mg/l, subinhibitory for strain MG1655 (pHly152), generation of Hly- clones could be readily detected. Similar results were also obtained when, instead of km, ampicillin was used. IS91 is flanking several virulence determinants in different enteric bacterial pathogenic strains from E. coli and Shigella. The results presented here evidence that stress generated by exposure to subinhibitory antibiotic concentrations may result in rearrangements of the bacterial genome. Whereas some of these rearrangements may be deleterious, others may generate genotypes with increased virulence, which may resume infection

The students' view

This year UKSG awarded six sponsored delegate places to students who had answered the call for applications.The following is an amalgam of excerpts from their reports on impressions and experiences of the 27th UKSG Annual Conference and Exhibition

Murine models for the study of fetal alcohol spectrum disorders: An overview

Prenatal alcohol exposure is associated to different physical, behavioral, cognitive, and neurological impairments collectively known as fetal alcohol spectrum disorder. The underlying mechanisms of ethanol toxicity are not completely understood. Experimental studies during human pregnancy to identify new diagnostic biomarkers are difficult to carry out beyond genetic or epigenetic analyses in biological matrices. Therefore, animal models are a useful tool to study the teratogenic effects of alcohol on the central nervous system and analyze the benefits of promising therapies. Animal models of alcohol spectrum disorder allow the analysis of key variables such as amount, timing and frequency of ethanol consumption to describe the harmful effects of prenatal alcohol exposure. In this review, we aim to synthetize neurodevelopmental disabilities in rodent fetal alcohol spectrum disorder phenotypes, considering facial dysmorphology and fetal growth restriction. We examine the different neurodevelopmental stages based on the most consistently implicated epigenetic mechanisms, cell types and molecular pathways, and assess the advantages and disadvantages of murine models in the study of fetal alcohol spectrum disorder, the different routes of alcohol administration, and alcohol consumption patterns applied to rodents. Finally, we analyze a wide range of phenotypic features to identify fetal alcohol spectrum disorder phenotypes in murine models, exploring facial dysmorphology, neurodevelopmental deficits, and growth restriction, as well as the methodologies used to evaluate behavioral and anatomical alterations produced by prenatal alcohol exposure in rodents.This work was supported by Red de Salud Materno-Infantil y del Desarrollo (SAMID) (RD12/0026/0003 and RD16/0022/0002) from Instituto de Salud Carlos III and the PI15/01179 grant from Instituto de Salud Carlos II

Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview

Prenatal alcohol exposure is associated to different physical, behavioral, cognitive, and neurological impairments collectively known as fetal alcohol spectrum disorder. The underlying mechanisms of ethanol toxicity are not completely understood. Experimental studies during human pregnancy to identify new diagnostic biomarkers are difficult to carry out beyond genetic or epigenetic analyses in biological matrices. Therefore, animal models are a useful tool to study the teratogenic effects of alcohol on the central nervous system and analyze the benefits of promising therapies. Animal models of alcohol spectrum disorder allow the analysis of key variables such as amount, timing and frequency of ethanol consumption to describe the harmful effects of prenatal alcohol exposure. In this review, we aim to synthetize neurodevelopmental disabilities in rodent fetal alcohol spectrum disorder phenotypes, considering facial dysmorphology and fetal growth restriction. We examine the different neurodevelopmental stages based on the most consistently implicated epigenetic mechanisms, cell types and molecular pathways, and assess the advantages and disadvantages of murine models in the study of fetal alcohol spectrum disorder, the different routes of alcohol administration, and alcohol consumption patterns applied to rodents. Finally, we analyze a wide range of phenotypic features to identify fetal alcohol spectrum disorder phenotypes in murine models, exploring facial dysmorphology, neurodevelopmental deficits, and growth restriction, as well as the methodologies used to evaluate behavioral and anatomical alterations produced by prenatal alcohol exposure in rodents

Murine Models for the Study of Fetal Alcohol Spectrum Disorders: An Overview.

Prenatal alcohol exposure is associated to different physical, behavioral, cognitive, and neurological impairments collectively known as fetal alcohol spectrum disorder. The underlying mechanisms of ethanol toxicity are not completely understood. Experimental studies during human pregnancy to identify new diagnostic biomarkers are difficult to carry out beyond genetic or epigenetic analyses in biological matrices. Therefore, animal models are a useful tool to study the teratogenic effects of alcohol on the central nervous system and analyze the benefits of promising therapies. Animal models of alcohol spectrum disorder allow the analysis of key variables such as amount, timing and frequency of ethanol consumption to describe the harmful effects of prenatal alcohol exposure. In this review, we aim to synthetize neurodevelopmental disabilities in rodent fetal alcohol spectrum disorder phenotypes, considering facial dysmorphology and fetal growth restriction. We examine the different neurodevelopmental stages based on the most consistently implicated epigenetic mechanisms, cell types and molecular pathways, and assess the advantages and disadvantages of murine models in the study of fetal alcohol spectrum disorder, the different routes of alcohol administration, and alcohol consumption patterns applied to rodents. Finally, we analyze a wide range of phenotypic features to identify fetal alcohol spectrum disorder phenotypes in murine models, exploring facial dysmorphology, neurodevelopmental deficits, and growth restriction, as well as the methodologies used to evaluate behavioral and anatomical alterations produced by prenatal alcohol exposure in rodents