Experimental exposure of the blue mussel (Mytilus edulis, L.) to the toxic dinoflagellate Alexandrium fundyense: Histopathology, immune responses, and recovery

Mussels (Mytilus edulis) were exposed to cultures of the toxic dinoflagellate Alexandrium fundyense or the non-toxic alga Rhodomonas sp. to evaluate the effects of the harmful alga on the mussels and to study recovery after discontinuation of the A. fundyense exposure. Mussels were exposed for 9 days to the different algae and then all were fed Rhodomonas sp. for 6 more days. Samples of hemolymph for hemocyte analyses and tissues for histology were collected before the exposure and periodically during exposure and recovery periods. Mussels filtered and ingested both microalgal cultures, producing fecal pellets containing degraded, partially degraded, and intact cells of both algae. Mussels exposed to A. fundyense had an inflammatory response consisting of degranulation and diapedesis of hemocytes into the alimentary canal and, as the exposure continued, hemocyte migration into the connective tissue between the gonadal follicles. Evidence of lipid peroxidation, similar to the detoxification pathway described for various xenobiotics, was found; insoluble lipofuchsin granules formed (ceroidosis), and hemocytes carried the granules to the alimentary canal, thus eliminating putative dinoflagellate toxins in feces. As the number of circulating hemocytes in A. fundyense-exposed mussels became depleted, mussels were immunocompromised, and pathological changes followed, i.e., increased prevalences of ceroidosis and trematodes after 9 days of exposure. Moreover, the total number of pathological changes increased from the beginning of the exposure until the last day (day 9). After 6 days of the exposure, mussels in one of the three tanks exposed to A. fundyense mass spawned; these mussels showed more severe effects of the toxic algae than non-spawning mussels exposed to A. fundyense. No significant differences were found between the two treatments during the recovery period, indicating rapid homeostatic processes in tissues and circulating hemocytes.

Com coneixen Descartes i Hume? : Una petita història del coneixement i les seves conseqüències contemporànies

És una anàlisi sobre el problema del coneixement als segles XVII (racionalisme) i XVIII (empirisme) i la seva influència en l'epistemologia contemporània. En concret, es comparen les teories del coneixement de René Descartes i de David Hume, es demostra la seva vigència al segle XXI i es proposa una aplicació extrafilosòfica al seu pensament.

Discourse, knowledge, power and politics: towards critical epistemic discourse analysis

Although both are fundamental terms in the humanities and social sciences, discourse and knowledge have seldom been explicitly related, and even less so in critical discourse studies. After a brief summary of what we know about these relationships in linguistics, psychology, epistemology and the social sciences, with special emphasis on the role of knowledge in the formation of mental models as a basis for discourse, I examine in more detail how a critical study of discourse and knowledge may be articulated in critical discourse studies. Thus, several areas of critical epistemic discourse analysis are identified, and then applied in a study of Tony Blair’s Iraq speech on March 18, 2003, in which he sought to legitimatize his decision to go to war in Iraq with George Bush. The analysis shows the various modes of how knowledge is managed and manipulated of all levels of discourse of this speech.

Regulation of GABA(A) and glutamate receptor expression, synaptic facilitation and long-term potentiation in the hippocampus of prion mutant mice

Background: Prionopathies are characterized by spongiform brain degeneration, myoclonia, dementia, and periodic electroencephalographic (EEG) disturbances. The hallmark of prioniopathies is the presence of an abnormal conformational isoform (PrP(sc)) of the natural cellular prion protein (PrP(c)) encoded by the Prnp gene. Although several roles have been attributed to PrP(c), its putative functions in neuronal excitability are unknown. Although early studies of the behavior of Prnp knockout mice described minor changes, later studies report altered behavior. To date, most functional PrP(c) studies on synaptic plasticity have been performed in vitro. To our knowledge, only one electrophysiological study has been performed in vivo in anesthetized mice, by Curtis and coworkers. They reported no significant differences in paired-pulse facilitation or LTP in the CA1 region after Schaffer collateral/commissural pathway stimulation. Principal Findings: Here we explore the role of PrP(c) expression in neurotransmission and neural excitability using wild-type, Prnp -/- and PrP(c)-overexpressing mice (Tg20 strain). By correlating histopathology with electrophysiology in living behaving mice, we demonstrate that both Prnp -/- mice but, more relevantly Tg20 mice show increased susceptibility to KA, leading to significant cell death in the hippocampus. This finding correlates with enhanced synaptic facilitation in paired-pulse experiments and hippocampal LTP in living behaving mutant mice. Gene expression profiling using Illumina microarrays and Ingenuity pathways analysis showed that 129 genes involved in canonical pathways such as Ubiquitination or Neurotransmission were co-regulated in Prnp -/- and Tg20 mice. Lastly, RT-qPCR of neurotransmission-related genes indicated that subunits of GABA(A) and AMPA-kainate receptors are co-regulated in both Prnp -/- and Tg20 mice. Conclusions/Significance: Present results demonstrate that PrP(c) is necessary for the proper homeostatic functioning of hippocampal circuits, because of its relationships with GABA(A) and AMPA-Kainate neurotransmission. New PrP(c) functions have recently been described, which point to PrP(c) as a target for putative therapies in Alzheimer's disease. However, our results indicate that a "gain of function" strategy in Alzheimer's disease, or a "loss of function" in prionopathies, may impair PrP(c) function, with devastating effects. In conclusion, we believe that present data should be taken into account in the development of future therapies.

Pro-inflammatory gene expression and neurotoxic effects of activated microglia are attenuated by absence of CCAAT/enhancer binding protein beta

Background. Microglia and astrocytes respond to homeostatic disturbances with profound changes of gene expression. This response, known as glial activation or neuroinflammation, can be detrimental to the surrounding tissue. The transcription factor CCAAT/enhancer binding protein ß (C/EBPß) is an important regulator of gene expression in inflammation but little is known about its involvement in glial activation. To explore the functional role of C/EBPß in glial activation we have analyzed pro-inflammatory gene expression and neurotoxicity in murine wild type and C/EBPß-null glial cultures. Methods. Due to fertility and mortality problems associated with the C/EBPß-null genotype we developed a protocol to prepare mixed glial cultures from cerebral cortex of a single mouse embryo with high yield. Wild-type and C/EBPß-null glial cultures were compared in terms of total cell density by Hoechst-33258 staining; microglial content by CD11b immunocytochemistry; astroglial content by GFAP western blot; gene expression by quantitative real-time PCR, western blot, immunocytochemistry and Griess reaction; and microglial neurotoxicity by estimating MAP2 content in neuronal/microglial cocultures. C/EBPß DNA binding activity was evaluated by electrophoretic mobility shift assay and quantitative chromatin immunoprecipitation. Results. C/EBPß mRNA and protein levels, as well as DNA binding, were increased in glial cultures by treatment with lipopolysaccharide (LPS) or LPS + interferon ¿ (IFN¿). Quantitative chromatin immunoprecipitation showed binding of C/EBPß to pro-inflammatory gene promoters in glial activation in a stimulus- and gene-dependent manner. In agreement with these results, LPS and LPS+IFN¿ induced different transcriptional patterns between pro-inflammatory cytokines and NO synthase-2 genes. Furthermore, the expressions of IL-1ß and NO synthase-2, and consequent NO production, were reduced in the absence of C/EBPß. In addition, neurotoxicity elicited by LPS+IFN¿-treated microglia co-cultured with neurons was completely abolished by the absence of C/EBPß in microglia.

E2F1 regulates cellular growth by mTOR signaling

During cell proliferation, growth must occur to maintain homeostatic cell size. Here we show that E2F1 is capable of inducing growth by regulating mTORC1 activity. The activation of cell growth and mTORC1 by E2F1 is dependent on both E2F1's ability to bind DNA and to regulate gene transcription, demonstrating that a gene induction expression program is required in this process. Unlike E2F1, E2F3 is unable to activate mTORC1, suggesting that growth activity could be restricted to individual E2F members. The effect of E2F1 on the activation of mTORC1 does not depend on Akt. Furthermore, over-expression of TSC2 does not interfere with the effect of E2F1, indicating that the E2F1-induced signal pathway can compensate for the inhibitory effect of TSC2 on Rheb. Immunolocalization studies demonstrate that E2F1 induces the translocation of mTORC1 to the late endosome vesicles, in a mechanism dependent of leucine. E2F1 and leucine, or insulin, together affect the activation of S6K stronger than alone suggesting that they are complementary in activating the signal pathway. From these studies, E2F1 emerges as a key protein that integrates cell division and growth, both of which are essential for cell proliferation.

El origen de la construcción fenomenalista: Mach, Moore y Whitehead

It's usually believed that the idea of applying logical methods to constructivist phenomenalism was, --in general- a result of Russell's originality. In this paper is argued that some important ideas were in fact due to Mach, Moore and Whitehead. According to the author, Russell got from Mach the general idea of epistemology as an analysis of scientific concepts and, specially,the idea of sensations as the building blocks for his logical construction. Moore made Russell believe that only sensations are known in a direct way, and so, the existence of external objects as the cause of our perceptions is only inferred. Moreover, according to the author, Russell's views on sense data -his sensibilia- are also due to Moore. Finally, Russell got from Whitehead the idea of the phenomenical reconstruction as an alternative to the causal theory of perception, and also how the logical construction should be done. The author undertakes also a detailed analysis of some early works of Whitehead not very well known.

Historias de vida en educación: biografías en contexto

[spa] Esta publicación recoge los trabajos presentados en las I Jornadas de Historias de Vida en Educación: Cuestiones epistemológicas, metodológicas, éticas y de formación que, organizadas por el grupo de investigación consolidado ESBRINA (Subjetividades y entornos educativos contemporáneos -2009SGR 503), se celebraron en el Departamento de Didáctica y Organización Educativa de la Universidad de Barcelona los días 10 y 11 de junio de 2010.A las mismas asistieron unas 50 personas -docentes e investigadores universitarios y estudiantes de máster y doctorado de España, Portugal, México, Chile, Italia, Francia y Brasil- quienes, después de una introducción por parte de las personas que coordinaban los temas, debatieron con intensidad las cuestiones que emergieron de la lectura de las contribuciones que algunos de los participantes enviaron previamente. Con posterioridad, la mayoría revisaron sus presentaciones para acomodarla al formato de esta publicación.

Historias de vida en educación: biografías en contexto

[spa] Esta publicación recoge los trabajos presentados en las I Jornadas de Historias de Vida en Educación: Cuestiones epistemológicas, metodológicas, éticas y de formación que, organizadas por el grupo de investigación consolidado ESBRINA (Subjetividades y entornos educativos contemporáneos -2009SGR 503), se celebraron en el Departamento de Didáctica y Organización Educativa de la Universidad de Barcelona los días 10 y 11 de junio de 2010.A las mismas asistieron unas 50 personas -docentes e investigadores universitarios y estudiantes de máster y doctorado de España, Portugal, México, Chile, Italia, Francia y Brasil- quienes, después de una introducción por parte de las personas que coordinaban los temas, debatieron con intensidad las cuestiones que emergieron de la lectura de las contribuciones que algunos de los participantes enviaron previamente. Con posterioridad, la mayoría revisaron sus presentaciones para acomodarla al formato de esta publicación.

Historias de vida en educación: biografías en contexto

[spa] Esta publicación recoge los trabajos presentados en las I Jornadas de Historias de Vida en Educación: Cuestiones epistemológicas, metodológicas, éticas y de formación que, organizadas por el grupo de investigación consolidado ESBRINA (Subjetividades y entornos educativos contemporáneos -2009SGR 503), se celebraron en el Departamento de Didáctica y Organización Educativa de la Universidad de Barcelona los días 10 y 11 de junio de 2010.A las mismas asistieron unas 50 personas -docentes e investigadores universitarios y estudiantes de máster y doctorado de España, Portugal, México, Chile, Italia, Francia y Brasil- quienes, después de una introducción por parte de las personas que coordinaban los temas, debatieron con intensidad las cuestiones que emergieron de la lectura de las contribuciones que algunos de los participantes enviaron previamente. Con posterioridad, la mayoría revisaron sus presentaciones para acomodarla al formato de esta publicación.

JNK controls the onset of mitosis of planarian stem cells and triggers apoptotic cell death required for regeneration and remodeling

Regeneration of lost tissues depends on the precise interpretation of molecular signals that control and coordinate the onset of proliferation, cellular differentiation and cell death. However, the nature of those molecular signals and the mechanisms that integrate the cellular responses remain largely unknown. The planarian flatworm is a unique model in which regeneration and tissue renewal can be comprehensively studied in vivo. The presence of a population of adult pluripotent stem cells combined with the ability to decode signaling after wounding enable planarians to regenerate a complete, correctly proportioned animal within a few days after any kind of amputation, and to adapt their size to nutritional changes without compromising functionality. Here, we demonstrate that the stress-activated c-jun-NH2-kinase (JNK) links wound-induced apoptosis to the stem cell response during planarian regeneration. We show that JNK modulates the expression of wound-related genes, triggers apoptosis and attenuates the onset of mitosis in stem cells specifically after tissue loss. Furthermore, in pre-existing body regions, JNK activity is required to establish a positive balance between cell death and stem cell proliferation to enable tissue renewal, remodeling and the maintenance of proportionality. During homeostatic degrowth, JNK RNAi blocks apoptosis, resulting in impaired organ remodeling and rescaling. Our findings indicate that JNK-dependent apoptotic cell death is crucial to coordinate tissue renewal and remodeling required to regenerate and to maintain a correctly proportioned animal. Hence, JNK might act as a hub, translating wound signals into apoptotic cell death, controlled stem cell proliferation and differentiation, all of which are required to coordinate regeneration and tissue renewal.