Media analysis and critical correspondences

Hemos visto la pequeña batalla de los intelectuales europeos, sus pronósticos derivados de la observación de la pandemia. La sopa de Wuhan, los anuncios de los más enfervorizados sobre el fin del capitalismo, las aseveraciones sobre que nada será igual una vez superada la misma, y también los rechazos a esta posiciones, la advertencia acerca de que la situación inmediata a la aparición de este ataque de la naturaleza a la fragilidad de la vida humana no variará, solo se verá estremecida, desconcertada y humillada.Facultad de Periodismo y Comunicación Socia

Modelos de crecimiento y producción en España: historia, ejemplos contemporáneos y perspectivas

En el presente trabajo se presenta una revisión sobre los modelos forestales desarrollados en España durante los últimos años, tanto para la producción maderable como no maderable y, para la dinámica de los bosques (regeneración, mortalidad). Se presentan modelos tanto de rodal completo como de clases diamétricas y de árbol individual. Los modelos desarrollados hasta la fecha se han desarrollado a partir de datos procedentes de parcelas permanentes, ensayos y el Inventario Forestal Nacional. En el trabajo se muestran los diferentes submodelos desarrollados hasta la fecha, así como las plataformas informáticas que permiten utilizar dichos modelos. Se incluyen las principales perspectivas de desarrollo de la modelización forestal en España.In this paper we present a review of forest models developed in Spain in recent years for both timber and non timber production and forest dynamics (regeneration, mortality). Models developed are whole stand, size (diameter) class and individual-tree. The models developed to date have been developed using data from permanent plots, experimental sites and the National Forest Inventory. In this paper we show the different sub-models developed so far and the friendly use software. Main perspectives of forest modeling in Spain are presented.The models described in this paper were funded by different regional, national and European projects, and some of them were elaborated by the authors. This work was funded by the Spanish Government by the SELVIRED network (code AGL2008-03740) and the strategic project «Restauración y Gestión Forestal» (code PSE-310000-2009-4)

Pathogen-Mediated Proteolysis of the Cell Death Regulator RIPK1 and the Host Defense Modulator RIPK2 in Human Aortic Endothelial Cells

Porphyromonas gingivalis is the primary etiologic agent of periodontal disease that is associated with other human chronic inflammatory diseases, including atherosclerosis. The ability of P. gingivalis to invade and persist within human aortic endothelial cells (HAEC) has been postulated to contribute to a low to moderate chronic state of inflammation, although how this is specifically achieved has not been well defined. In this study, we demonstrate that P. gingivalis infection of HAEC resulted in the rapid cleavage of receptor interacting protein 1 (RIPK1), a mediator of tumor necrosis factor (TNF) receptor-1 (TNF-R1)-induced cell activation or death, and RIPK2, a key mediator of both innate immune signaling and adaptive immunity. The cleavage of RIPK1 or RIPK2 was not observed in cells treated with apoptotic stimuli, or cells stimulated with agonists to TNF-R1, nucleotide oligomerization domain receptor 1(NOD1), NOD2, Toll-like receptor 2 (TLR2) or TLR4. P. gingivalis-induced cleavage of RIPK1 and RIPK2 was inhibited in the presence of a lysine-specific gingipain (Kgp) inhibitor. RIPK1 and RIPK2 cleavage was not observed in HAEC treated with an isogenic mutant deficient in the lysine-specific gingipain, confirming a role for Kgp in the cleavage of RIPK1 and RIPK2. Similar proteolysis of poly (ADP-ribose) polymerase (PARP) was observed. We also demonstrated direct proteolysis of RIPK2 by P. gingivalis in a cell-free system which was abrogated in the presence of a Kgp-specific protease inhibitor. Our studies thus reveal an important role for pathogen-mediated modification of cellular kinases as a potential strategy for bacterial persistence within target host cells, which is associated with low-grade chronic inflammation, a hallmark of pathogen-mediated chronic inflammatory disorders

CIBERER : Spanish national network for research on rare diseases: A highly productive collaborative initiative

Altres ajuts: Instituto de Salud Carlos III (ISCIII); Ministerio de Ciencia e Innovación.CIBER (Center for Biomedical Network Research; Centro de Investigación Biomédica En Red) is a public national consortium created in 2006 under the umbrella of the Spanish National Institute of Health Carlos III (ISCIII). This innovative research structure comprises 11 different specific areas dedicated to the main public health priorities in the National Health System. CIBERER, the thematic area of CIBER focused on rare diseases (RDs) currently consists of 75 research groups belonging to universities, research centers, and hospitals of the entire country. CIBERER's mission is to be a center prioritizing and favoring collaboration and cooperation between biomedical and clinical research groups, with special emphasis on the aspects of genetic, molecular, biochemical, and cellular research of RDs. This research is the basis for providing new tools for the diagnosis and therapy of low-prevalence diseases, in line with the International Rare Diseases Research Consortium (IRDiRC) objectives, thus favoring translational research between the scientific environment of the laboratory and the clinical setting of health centers. In this article, we intend to review CIBERER's 15-year journey and summarize the main results obtained in terms of internationalization, scientific production, contributions toward the discovery of new therapies and novel genes associated to diseases, cooperation with patients' associations and many other topics related to RD research

TRY plant trait database – enhanced coverage and open access

Plant traits - the morphological, anatomical, physiological, biochemical and phenological characteristics of plants - determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait‐based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits - almost complete coverage for ‘plant growth form’. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait–environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

<i>P. gingivalis</i>-induced proteolysis of RIPK proteins is dose-dependent and heat labile.

<p>HAEC were treated with medium (<b>M</b>), live <i>P. gingivalis</i> strain 381 (MOI 10) (<b>10</b>), live <i>P. gingivalis</i> (MOI 100) (<b>100</b>), heat-killed (HK) (60°C, 60 min) <i>P. gingivalis</i> 381 (MOI 100 equivalency) (<b>60°</b>), or with HK (80°C, 20 min) <i>P. gingivalis</i> 381 (MOI 100 equivalency) (<b>80°</b>) for 2 h. Whole cell lysates were analyzed for the detection of RIPK1 (left panel) or RIPK2 (right panel). Full-length RIPK1 and RIPK2 are indicated with arrows. Prominent <i>P. gingivalis</i>-induced LMW bands are indicated with asterisk(s). MW ladder is indicated on the left in kDa. GAPDH was detected as a loading control.</p

Model of <i>P. gingivalis</i> innate immune activation/invasion in endothelial cells.

<p>Outcome of innate immune responses is representative as a balance of functional, intact pathways (TLR-left panel) and dysregulated pathways (NLR-right panel). <i>P. gingivalis</i> represents a human pathogen that utilizes fimbriae for attachment and invasion of endothelial cells. Fimbriae are not only expressed on whole bacteria (<b>A</b>), but within outer membrane vesicles (OMV) that are released from the cell (<b>B</b>), as occurs with all Gram-negative bacteria identified to date. Fimbriae bind to TLR2 and MD2 to activate TLR2 and TLR4, resulting in the induction of NF-κB, leading to inflammation, and <i>de novo</i> protein synthesis (<b>C</b>) of cell adhesion molecules (<b>CAM</b>) and TLR (<b>TLR</b>) expressed at the cell surface (<b>D</b>). Many studies have demonstrated invasion of endothelial cells by <i>P. gingivalis</i> (<b>E</b>). However, recent studies have shown that OMV (containing fimbriae and active gingipain activity) gain entry into host cells rapidly in a gingipain-dependent manner (<b>E</b>), independent of whole organism. Upon entry, intracellular gingipain activity degrades RIPK1 and RIPK2 (abrogated by protease inhibitors) (<b>F</b>), resulting in a variety of possible consequences as a function of selective targeting of intracellular NOD1 or NOD2 (NOD1/2) signaling pathways and/or disruption of RIPK1 or RIPK2-mediated cell signaling. Alteration of immune signaling responses may result in decreased host cell death, decreased inflammatory mediator expression, and subsequent enhancement of intracellular bacterial cell survival, all of which contributes to an intracellular niche for <i>P. gingivalis</i> (<b>G</b>).</p

General caspase inhibitors z-VAD-FMK and Boc-D-FMK alter <i>P. gingivalis</i>-induced modification of RIPK1 and RIPK2 in HUVEC.

<p>HUVEC were pretreated (Pre-Tx) with medium (<b>M</b>), 0.25% DMSO vehicle control (<b>C</b>), 25 µM z-VAD-FMK (<b>VAD</b>), or 100 µM Boc-D-FMK (<b>Boc</b>) with for 1.5 h. HUVEC were then treated with medium (<b>M</b>) or <i>P. gingivalis</i> strain 381 (MOI 100, <b>381</b>) for 2 h. Whole cell lysates were analyzed for (<b>A</b>) RIPK1 or (<b>B</b>) RIPK2 and GAPDH. Full-length RIPK1 and RIPK2 are indicated with arrows. Prominent <i>P. gingivalis</i>-induced LMW bands are indicated with asterisks. MW ladder is indicated on the left in kDa.</p

<i>P. gingivalis</i> 381-induced proteolysis of RIPK1 and RIPK2 in HAEC.

<p>HAEC were treated with medium (<b>M</b>) or with <i>P. gingivalis</i> strain 381 (MO1 100) for 0.25, 0.5, 1, 2, 6, 12, 24 or 48 h. Whole cell lysates were analyzed for the detection of <b>A</b>) RIPK1, <b>B</b>) RIPK2 with an anti N′-terminal RIPK2 antibody (left panel) or an anti C′-terminal RIPK2 antibody (right panel), or <b>C</b>) NOD1 (left panel) and NOD2 (right panel). Full-length RIPK1 (74-kDa) and RIPK2 (61-kDa) are indicated with arrows. Prominent <i>P. gingivalis</i>-induced LMW bands are indicated with asterisks. Molecular weight (MW) ladder is indicated on the left in kDa. GAPDH was detected as a loading control. (−) protein levels in medium-treated cells were similar at all time points. Densitometric analysis is presented below respective blots as the mean (+/− SEM) ratio of NOD1 (or NOD2) to GAPDH protein levels (arbitrary densitometric units (A.D.U.) from at least 3 independent membranes. Means are displayed within the bar charts.</p