Key plant species and detritivores drive diversity effects on instream leaf litter decomposition more than functional diversity: A microcosm study.

Anthropogenic impacts on freshwater ecosystems cause critical losses of biodiversity that can in turn impair key processes such as decomposition and nutrient cycling. Forest streams are mainly subsidized by terrestrial organic detritus, so their functioning and conservation status can be altered by changes in forest biodiversity and composition, particularly if these changes involve the replacement of functional groups or the loss of key species. We examined this issue using a microcosm experiment where we manipulated plant functional diversity (FD) (monocultures and low-FD and high-FD mixtures, resulting from different combinations of deciduous and evergreen Quercus species) and the presence of a key species (Alnus glutinosa), all in presence and absence of detritivores, and assessed effects on litter decomposition, nutrient cycling, and fungal and detritivore biomass. We found (i) positive diversity effects on detritivore-mediated decomposition, litter nutrient losses and detritivore biomass exclusively when A. glutinosa was present; and (ii) negative effects on the same processes when microbially mediated and on fungal biomass. Most positive trends could be explained by the higher litter palatability and litter trait variability obtained with the inclusion of alder leaves in the mixture. Our results support the hypothesis of a consistent slowing down of the decomposition process as a result of plant biodiversity loss, and hence effects on stream ecosystem functioning, especially when a key (N-fixing) species is lost; and underscore the importance of detritivores as drivers of plant diversity effects in the studied ecosystem processes.

Animal models for neurotoxicity assessment in cardiac arrest / Modelos animales para evaluar la neurotoxicidad en el paro cardíaco

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Principales modelos experimentales de traumatismo craneoencefálico: de la preclínica a los modelos in vitro / Experimental models in traumatic brain injury: from animal models to in vitro assays

El traumatismo craneoencefálico (TCE) es una de las patologías más importantes en la actualidad, ya que afecta a un alto porcentaje de individuos de todas las edades. A pesar de los avances en el campo del diagnóstico, la monitorización y el tratamiento del TCE, quedan importantes cuestiones sin resolver alrededor de la fisiopatología de este tipo de traumatismo. Con el fin de profundizar en dicho conocimiento y poder evaluar y aplicar un posible tratamiento que resulte eficaz para estos pacientes, se han desarrollado diferentes modelos experimentales que simulan los mecanismos de acción y el cuadro clínico del TCE. A su vez, cada modelo representa un determinado tipo de traumatismo y evalúa un aspecto concreto de la cascada fisiopatológica desencadenada tras el TCE. El objetivo de este trabajo es detallar los principales modelos experimentales que abordan la lesión cerebral tras un TCE, así como su potencial traslación a la práctica clínica diaria

Traumatic brain Injury (TBI) is a major public healthcare concern, affecting people of all ages. Despite advances in the diagnosis, monitoring and clinical management of TBI, many unresolved questions remain regarding its physiopathology. In an attempt to understand the pathological features of TBI and to evaluate single potential therapeutic strategies, various animal models have been developed to simulate the mechanisms of action and the clinical manifestations of TBI patients. In turn, each model represents a specific type of trauma and evaluates a specific physiopathological aspect of the cascade triggered as a result of TBI. This review describes the main experimental models currently available referred to TBI and their possible application to the clinical setting

Correction to: BRG1 regulation by miR-155 in human leukemia and lymphoma cell lines.

Following the publication of the original article the author listed as Antonio Herrera contacted the Publisher to state that his correct and full name is Antonio Herrera-Merchan. Antonio Herrera-Merchan has agreed to the publication of this erratum.

Experimental models in traumatic brain injury: from animal models to in vitro assays. / Principales modelos experimentales de traumatismo craneoencefálico: de la preclínica a los modelos in vitro.

Traumatic brain Injury (TBI) is a major public healthcare concern, affecting people of all ages. Despite advances in the diagnosis, monitoring and clinical management of TBI, many unresolved questions remain regarding its physiopathology. In an attempt to understand the pathological features of TBI and to evaluate single potential therapeutic strategies, various animal models have been developed to simulate the mechanisms of action and the clinical manifestations of TBI patients. In turn, each model represents a specific type of trauma and evaluates a specific physiopathological aspect of the cascade triggered as a result of TBI. This review describes the main experimental models currently available referred to TBI and their possible application to the clinical setting.

BRG1 regulation by miR-155 in human leukemia and lymphoma cell lines

Introduction/purpose. BRG1 is a key regulator of leukemia stem cells. Indeed, it has been observed that this type of cells is unable to divide, survive and develop new tumors when BRG1 is down-regulated. Materials and methods. We assessed BRG1 and miR-155 expression in 23 leukemia cell lines, and two no pathological lymphocyte samples using qPCR. MiR-155 transfection and western blot were used to analyze the relationship between miR-155 and its validated target, BRG1, by measuring protein expression levels. The effect of miR-155 on cell proliferation and prednisolone sensitivity were studied with resazurin assay. Results. BRG1 expression levels could correlate negatively with miR-155 expression levels, at least in Burkitt’s lymphoma and diffuse large B cell lymphoma (DLBCL) cell lines. To clarify the role of miR-155 in the regulation of BRG1 expression, we administrated miR-155 mimics in different leukemia/lymphoma cell lines. Our results suggest that miR-155 regulate negatively and significantly the BRG1 expression at least in the MOLT4 cell line. Conclusion. Our study revealed a previously unknown miR-155 heterogeneity that could result in differences in the treatment with miRNAs in our attempt to inhibit BRG1. However, the expression levels of BRG1 and miR-155, before prednisolone treatment were not statistically significantly associated prednisolone sensitive leukemia cells (AU)

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BRG1 regulation by miR-155 in human leukemia and lymphoma cell lines.

INTRODUCTION/PURPOSE: BRG1 is a key regulator of leukemia stem cells. Indeed, it has been observed that this type of cells is unable to divide, survive and develop new tumors when BRG1 is down-regulated. MATERIALS AND METHODS: We assessed BRG1 and miR-155 expression in 23 leukemia cell lines, and two no pathological lymphocyte samples using qPCR. MiR-155 transfection and western blot were used to analyze the relationship between miR-155 and its validated target, BRG1, by measuring protein expression levels. The effect of miR-155 on cell proliferation and prednisolone sensitivity were studied with resazurin assay. RESULTS: BRG1 expression levels could correlate negatively with miR-155 expression levels, at least in Burkitt's lymphoma and diffuse large B cell lymphoma (DLBCL) cell lines. To clarify the role of miR-155 in the regulation of BRG1 expression, we administrated miR-155 mimics in different leukemia/lymphoma cell lines. Our results suggest that miR-155 regulate negatively and significantly the BRG1 expression at least in the MOLT4 cell line. CONCLUSION: Our study revealed a previously unknown miR-155 heterogeneity that could result in differences in the treatment with miRNAs in our attempt to inhibit BRG1. However, the expression levels of BRG1 and miR-155, before prednisolone treatment were not statistically significantly associated prednisolone sensitive leukemia cells.