51 resultados para Ancestral Mediator
Resumo:
Palaeobotany applied to freshwater plants is an emerging field of palaeontology. Hydrophytic plants reveal evolutionary trends of their own, clearly distinct from those of the terrestrial and marine flora. During the Precambrian, two groups stand out in the fossil record of freshwater plants: the Cyanobacteria (stromatolites) in benthic environments and the prasinophytes (leiosphaeridian acritarchs) in transitional planktonic environments. During the Palaeozoic, green algae (Chlorococcales, Zygnematales, charophytes and some extinct groups) radiated and developed the widest range of morphostructural patterns known for these groups. Between the Permian and Early Cretaceous, charophytes dominated macrophytic associations, with the consequence that over tens of millions of years, freshwater flora bypassed the dominance of vascular plants on land. During the Early Cretaceous, global extension of the freshwater environments is associated with diversification of the flora, including new charophyte families and the appearance of aquatic angiosperms and ferns for the first time. Mesozoic planktonic assemblages retained their ancestral composition that was dominated by coenobial Chlorococcales, until the appearance of freshwater dinoflagellates in the Early Cretaceous. In the Late Cretaceous, freshwater angiosperms dominated almost all macrophytic communities worldwide. The Tertiary was characterised by the diversification of additional angiosperm and aquatic fern lineages, which resulted in the first differentiation of aquatic plant biogeoprovinces. Phytoplankton also diversified during the Eocene with the development of freshwater diatoms and chrysophytes. Diatoms, which were exclusively marine during tens of millions of years, were dominant over the Chlorococcales during Neogene and in later assemblages. During the Quaternary, aquatic plant communities suffered from the effects of eutrophication, paludification and acidification, which were the result of the combined impact of glaciation and anthropogenic disturbance.
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Planarians have been established as an ideal model organism for stem cell research and regeneration. Planarian regeneration and homeostasis require an exquisite balancing act between cell death and cell proliferation as new tissues are made (epimorphosis) and existing tissues remodeled (morphallaxis). Some of the genes and mechanisms that control cell proliferation and pattern formation are known. However, studies about cell death during remodeling are few and far between. We have studied the gene Gtdap-1, the planarian ortholog of human death-associated protein-1 or DAP-1. DAP-1 together with DAP-kinase has been identified as a positive mediator of programmed cell death induced by gamma-interferon in HeLa cells. We have found that the gene functions at the interface between autophagy and cell death in the remodeling of the organism that occurs during regeneration and starvation in sexual and asexual races of planarians. Our data suggest that autophagy of existing cells may be essential to fuel the continued proliferation and differentiation of stem cells by providing the necessary energy and building blocks to neoblasts.
Resumo:
Sacoglossan sea slugs (Mollusca: Opisthobranchia) are one of the few groups of specialist herbivores in the marine environment. Sacoglossans feed suctorially on the cell sap of macroalgae, from which they 'steal' chloroplasts (kleptoplasty) and deterrent substances (kleptochemistry), retaining intracellularly both host plastids and chemicals. The ingested chloroplasts continue to photosynthesize for periods ranging from a few hours or days up to 3 months in some species. Shelled, more primitive sacoglossans feed only on the siphonalean green algal genus Caulerpa, and they do not have functional kleptoplasty. The diet of sacoglossans has radiated out from this ancestral food. Among the shell-less Plakobranchidae (=Elysiidae), the more primitive species feed on other siphonales (families Derbesiaceae, Caulerpaceae, Bryopsidaceae and Codiaceae) and fix carbon, while the more 'advanced' species within the Plakobranchidae and Limapontioidae have a more broad dietary range. Most of these 'advanced' species are unable to fix carbon because the chloroplasts of their food algae are mechanically disrupted during ingestion. Mesoherbivores are likely to be eaten if they live on palatable seaweeds, their cryptic coloration and form not always keeping them safe from predators. Sacoglossans prefer to live on and eat chemically defended seaweeds, and they use ingested algal chemicals as deterrents of potential predators. The most ancestral shelled sacoglossans (Oxynoidae) and some Plakobranchidae such as Elysia translucens, Thuridilla hopei and Bosellia mimetica have developed a diet-derived chemical defense mechanism. Oxynoids and Thuridilla hopei are able to biomodify the algal metabolites. However, the Plakobranchidae Elysia timida and E. viridis, together with Limapontioidea species, are characterized by their ability to de novo synthesize polypropionate metabolites. A whole analysis of kleptoplasty and chemical defenses in sacoglossans may offer a better understanding of the ecology and evolution of these specialized opisthobranchs. In this paper we summarize some of the latest findings, related mainly to Mediterranean species, and offer a plausible evolutionary scenario based on the biological and chemical trends we can distinguish in them.
Resumo:
Se han medido las variables métricas de la dentición del yacimiento de época mesolítica (7500-6500 a.C.), procedentes del yacimiento de La Oliva (Valencia) y se han comparado con las de otras poblaciones prehistóricas. Estas variables permiten situar esta población en el contexto europeo y extrapolar, mediante el análisis de árboles filogenéticos, los movimientos y relaciones poblacionales del Neolítico en Europa. De esta forma se observa que La Oliva forma parte de un antiguo grupo poblacional ancestral, bastante distanciado de las poblaciones mesolíticas contemporáneas del resto de Europa y de las poblaciones neolíticas posteriores. Parece, a su vez, que estas poblaciones neolíticas las substituirían casi completamente sin mestizaje aparente. Estos resultados se han contrastado y contrastado mediante análisis de variables métricas craneales.
Resumo:
Background: It has been shown in a variety of organisms, including mammals, that genes that appeared recently in evolution, for example orphan genes, evolve faster than older genes. Low functional constraints at the time of origin of novel genes may explain these results. However, this observation has been recently attributed to an artifact caused by the inability of Blast to detect the fastest genes in different eukaryotic genomes. Distinguishing between these two possible explanations would be of great importance for any studies dealing with the taxon distribution of proteins and the origin of novel genes. Results: Here we used simulations of protein sequences to examine the capacity of Blast to detect proteins of diverse evolutionary rates in the different species of an eukaryotic phylogenetic tree that included metazoans, fungi and plants. We simulated the evolution of protein genes with the same evolutionary rates than those observed in functional mammalian genes and with among-site rate heterogeneity. Under these conditions, we found that only a very small percentage of simulated ancestral eukaryotic proteins was affected by the Blast artifact. We show that the good detectability of Blast is due to the heterogeneity of protein evolutionary rates at different sites, since only a small conserved motif in a sequence suffices to detect its homologues. Our results indicate that Blast, at least when applied within eukaryotes, only misses homologues of extremely fast-evolving sequences, which are rare in the mammalian genome, as well as sequences evolving homogeneously or pseudogenes.Conclusion: Although great care should be exercised in the recognition of remote homologues, most functional mammalian genes can be detected in eukaryotic genomes by Blast. That is, the majority of functional mammalian genes are not as fast as for not being detected in other metazoans, fungi or plants, if they had been present in these organisms. Thus, the correlation previously found between age and rate seems not to be due to a pure Blast artifact, at least for mammals. This may have important implications to understand the mechanisms by which novel genes originate.
Resumo:
Low-complexity regions (LCRs) in proteins are tracts that are highly enriched in one or a few aminoacids. Given their high abundance, and their capacity to expand in relatively short periods of time through replication slippage, they can greatly contribute to increase protein sequence space and generate novel protein functions. However, little is known about the global impact of LCRs on protein evolution. We have traced back the evolutionary history of 2,802 LCRs from a large set of homologous protein families from H.sapiens, M.musculus, G.gallus, D.rerio and C.intestinalis. Transcriptional factors and other regulatory functions are overrepresented in proteins containing LCRs. We have found that the gain of novel LCRs is frequently associated with repeat expansion whereas the loss of LCRs is more often due to accumulation of amino acid substitutions as opposed to deletions. This dichotomy results in net protein sequence gain over time. We have detected a significant increase in the rate of accumulation of novel LCRs in the ancestral Amniota and mammalian branches, and a reduction in the chicken branch. Alanine and/or glycine-rich LCRs are overrepresented in recently emerged LCR sets from all branches, suggesting that their expansion is better tolerated than for other LCR types. LCRs enriched in positively charged amino acids show the contrary pattern, indicating an important effect of purifying selection in their maintenance. We have performed the first large-scale study on the evolutionary dynamics of LCRs in protein families. The study has shown that the composition of an LCR is an important determinant of its evolutionary pattern.
Resumo:
Climate change may pose challenges and opportunities to viticulture, and much research has focused in studying the likely impacts on grapes and wine production in different regions worldwide. This study assesses the vulnerability and adaptive capacity of the viticulture sector under changing climate conditions, based on a case study in El Penedès region, Catalonia. Farm assets, livelihood strategies, farmer-market interactions and climate changes perceptions are analysed through semi-structured interviews with different types of wineries and growers. Both types of actors are equally exposed to biophysical stressors but unevenly affected by socioeconomic changes. While wineries are vulnerable because of the current economic crisis and the lack of diversification of their work, which may affect their income or production, growers are mainly affected by the low prices of their products and the lack of fix contracts. These socioeconomic stressors strongly condition their capacity to adapt to climate change, meaning that growers prioritize their immediate income problems, rather than future socioeconomic or climate threats. Therefore, growers undertake reactive adaptation to climate changing conditions, mainly based on ancient knowledge, whilst wineries combine both reactive and anticipatory adaptation practices. These circumstances should be addressed in order to allow better anticipatory adaptation to be implemented, thus avoiding future climate threats.
Resumo:
We hypothesized that platelet-activating factor (PAF), a potent inflammatory mediator, could induce gas exchange abnormalities in normal humans. To this end, the effect of aerosolized PAF (2 mg/ml solution; 24 micrograms) on ventilation-perfusion (VA/Q) relationships, hemodynamics, and resistance of the respiratory system was studied in 14 healthy, nonatopic, and nonsmoking individuals (23 +/- 1 [SEM]yr) before and at 2, 4, 6, 8, 15, and 45 min after inhalation, and compared to that of inhaled lyso-PAF in 10 other healthy individuals (24 +/- 2 yr). PAF induced, compared to lyso-PAF, immediate leukopenia (P < 0.001) followed by a rebound leukocytosis (P < 0.002), increased minute ventilation (P < 0.05) and resistance of the respiratory system (P < 0.01), and decreased systemic arterial pressure (P < 0.05). Similarly, compared to lyso-PAF, PaO2 showed a trend to fall (by 12.2 +/- 4.3 mmHg, mean +/- SEM maximum change from baseline), and arterial-alveolar O2 gradient increased (by 16.7 +/- 4.3 mmHg) (P < 0.02) after PAF, because of VA/Q mismatch: the dispersion of pulmonary blood flow and that of ventilation increased by 0.45 +/- 0.1 (P < 0.01) and 0.29 +/- 0.1 (P < 0.04), respectively. We conclude that in normal subjects, inhaled PAF results in considerable immediate VA/Q inequality and gas exchange impairment. These results reinforce the notion that PAF may play a major role as a mediator of inflammation in the human lung.
Resumo:
We hypothesized that platelet-activating factor (PAF), a potent inflammatory mediator, could induce gas exchange abnormalities in normal humans. To this end, the effect of aerosolized PAF (2 mg/ml solution; 24 micrograms) on ventilation-perfusion (VA/Q) relationships, hemodynamics, and resistance of the respiratory system was studied in 14 healthy, nonatopic, and nonsmoking individuals (23 +/- 1 [SEM]yr) before and at 2, 4, 6, 8, 15, and 45 min after inhalation, and compared to that of inhaled lyso-PAF in 10 other healthy individuals (24 +/- 2 yr). PAF induced, compared to lyso-PAF, immediate leukopenia (P < 0.001) followed by a rebound leukocytosis (P < 0.002), increased minute ventilation (P < 0.05) and resistance of the respiratory system (P < 0.01), and decreased systemic arterial pressure (P < 0.05). Similarly, compared to lyso-PAF, PaO2 showed a trend to fall (by 12.2 +/- 4.3 mmHg, mean +/- SEM maximum change from baseline), and arterial-alveolar O2 gradient increased (by 16.7 +/- 4.3 mmHg) (P < 0.02) after PAF, because of VA/Q mismatch: the dispersion of pulmonary blood flow and that of ventilation increased by 0.45 +/- 0.1 (P < 0.01) and 0.29 +/- 0.1 (P < 0.04), respectively. We conclude that in normal subjects, inhaled PAF results in considerable immediate VA/Q inequality and gas exchange impairment. These results reinforce the notion that PAF may play a major role as a mediator of inflammation in the human lung.
Resumo:
Bipolar disorder (BD) is associated with substantial morbidity, as well as premature mortality. Available evidence indicates that 'stress-sensitive' chronic medical disorders, such as cardiovascular disease, obesity and Type 2 diabetes mellitus, are critical mediators and/or moderators of BD. Changes in physiologic systems implicated in allostasis have been proposed to impact brain structures and neurocognition, as well as medical comorbidity in this population. For example, abnormalities in insulin physiology, for example, insulin resistance, hyperinsulinemia and central insulinopenia, are implicated as effectors of allostatic load in BD. Insulin's critical role in CNS physiological (e.g., neurotrophism and synaptic plasticity) and pathophysiological (e.g., neurocognitive deficits, pro-apoptosis and amyloid deposition) processes is amply documented. This article introduces the concept that insulin is a mediator of allostatic load in the BD and possibly a therapeutic target.
Resumo:
Background: Chronic Obstructive Pulmonary Disease (COPD) is characterized by an enhanced inflammatory response to smoking that persists despite quitting. The resolution of inflammation (catabasis) is a complex and highly regulated process where tissue resident macrophages play a key role since they phagocytose apoptotic cells (efferocytosis), preventing their secondary necrosis and the spill-over of their pro-inflammatory cytoplasmic content, and release pro-resolution and tissue repair molecules, such as TGFβ, VEGF and HGF. Because inflammation does not resolve in COPD, we hypothesized that catabasis may be abnormal in these patients. Methods: To explore this hypothesis, we studied lung tissue samples obtained at surgery from 21 COPD patients,22 smokers with normal spirometry and 13 non-smokers controls. In these samples we used: (1)immunohistochemistry to assess the expression of CD44, CD36, VEGF and TGFβ in lung macrophages; (2) real time PCR to determine HGF, PPARγ, TGFβ, VEGF and MMP-9 gene expression; and, (3) ELISA to quantify lipoxin A4, a lipid mediator of catabasis. Results: We found that current and former smokers with COPD showed: (1) more inflammation (higher MMP-9 expression); (2) reduced macrophage surface expression of CD44, a key efferocytosis receptor; and, (3) similar levels of TGFβ, VEGF, HGF, PPARγ, and lipoxin A4 than smokers with normal spirometry, despite the presence of inflammation and disease. Conclusions: These results identify several potential abnormalities of catabasis in patients with COPD.
Resumo:
Nerve injuries often lead to neuropathic pain syndrome. The mechanisms contributing to this syndrome involve local inflammatory responses, activation of glia cells, and changes in the plasticity of neuronal nociceptive pathways. Cannabinoid CB(2) receptors contribute to the local containment of neuropathic pain by modulating glial activation in response to nerve injury. Thus, neuropathic pain spreads in mice lacking CB(2) receptors beyond the site of nerve injury. To further investigate the mechanisms leading to the enhanced manifestation of neuropathic pain, we have established expression profiles of spinal cord tissues from wild-type and CB(2)-deficient mice after nerve injury. An enhanced interferon-gamma (IFN-gamma) response was revealed in the absence of CB(2) signaling. Immunofluorescence stainings demonstrated an IFN-gamma production by astrocytes and neurons ispilateral to the nerve injury in wild-type animals. In contrast, CB(2)-deficient mice showed neuronal and astrocytic IFN-gamma immunoreactivity also in the contralateral region, thus matching the pattern of nociceptive hypersensitivity in these animals. Experiments in BV-2 microglia cells revealed that transcriptional changes induced by IFN-gamma in two key elements for neuropathic pain development, iNOS (inducible nitric oxide synthase) and CCR2, are modulated by CB(2) receptor signaling. The most direct support for a functional involvement of IFN-gamma as a mediator of CB(2) signaling was obtained with a double knock-out mouse strain deficient in CB(2) receptors and IFN-gamma. These animals no longer show the enhanced manifestations of neuropathic pain observed in CB(2) knock-outs. These data clearly demonstrate that the CB(2) receptor-mediated control of neuropathic pain is IFN-gamma dependent.
Resumo:
Different signatures of natural selection persist over varying time scales in our genome, revealing possible episodes of adaptative evolution during human history. Here, we identify genes showing signatures of ancestral positive selection in the human lineage and investigate whether some of those genes have been evolving adaptatively in extant human populations. Specifically, we compared more than 11,000 human genes with their orthologs inchimpanzee, mouse, rat and dog and applied a branch-site likelihood method to test for positive selection on the human lineage. Among the significant cases, a robust set of 11 genes were then further explored for signatures of recent positive selection using SNP data. We genotyped 223 SNPs in 39 worldwide populations from the HGDP Diversity panel and supplemented this information with available genotypes for up to 4,814 SNPs distributed along 2 Mb centered on each gene. After exploring the allele frequency spectrum, population differentiation and the maintainance of long unbroken haplotypes, we found signals of recent adaptative phenomena in only one of the 11 candidate gene regions. However, the signal ofrecent selection in this region may come from a different, neighbouring gene (CD5) ratherthan from the candidate gene itself (VPS37C). For this set of positively-selected genes in thehuman lineage, we find no indication that these genes maintained their rapid evolutionarypace among human populations. Based on these data, it therefore appears that adaptation forhuman-specific and for population-specific traits may have involved different genes.
Resumo:
La aproximación al tipo de mediación intercultural que se está llevando a cabo en Cataluña en este momento en el ámbito educativo -y su desarrollo futuro- se concreta y se dibuja en la diversidad de respuestas y de enfoques que aparecen del mismo término. Hemos intentado poner en común la reflexión y el debate sobre cuál sería la figura ideal y real del mediador intercultural. Con esta finalidad se han realizado 17 entrevistas a todos los coordinadores y formadores en ejercicio.
Resumo:
En Cataluña, en los últimos años, han ido proliferando una serie de "profesionales" que realizan, con más o menos adecuación a la definición teórica, la función de mediadores interculturales. Primeramente se trataba de gitanos, pero recientemente, fruto del incremento de la presencia de niños de origen inmigrante en las escuelas catalanas, se ha visto crecer el número y el protagonismo de los extranjeros por el reconocimiento que se les ha otorgado desde la administración y las instituciones. Al ser una práctica nueva está aún llena de interrogantes, pero al notar que no se está produciendo paralelamente una reflexión y clarificación de sus fundamentos nos parece que es un momento pertinente para examinar su desarrollo. Por ello hemos realizado una encuesta al profesorado de enseñanza obligatoria (n=740), que nos han proporcionado su percepción sobre la figura del mediador.