997 resultados para light adaptation


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[cat] Aquest treball recull el procés i els resultats de la recerca "Dones a la Ciència i a la Universitat: la contribució de la identitat docent i investigadora en contextos de desigualtat" (2007 RDG 00001)finançada per l'Agència de Gestió d'Ajuts Universitaris i de Recerca (AGAUR) en la convocatòria d'ajuts per a l'estudi de desigualtats originades per motius de gènere en l'àmbit científic i universitari (RDG) per l'any 2007. La finalitat d'aquest projecte ha estat explorar i reconstruirl'experiència personal i professional de tres generacions de dones en el procés de construcció de la seva identitat com a docents, investigadores i gestores. La forma d'assolir aquesta finalitat ha estatl'elaboració de 8 històries de vida professional per tal de comprendre la relació entre les seves trajectòries i les condicions de la seva feina i esbrinar com es van convertir en la mena de donesprofessores, investigadores o gestores que ara són; així com les relacions entre les experiències personals i el desenvolupament de les seves trajectòries professionals. En aquest procés s'han posat en evidència les estratègies d'adaptació, resistència i creació que les dones desenvolupen enla seva interacció amb el context de la docència, la recerca i la gestió, les formes de violència simbòlica que experimenten, i els canvis que s'han produït al centres de recerca i les universitats catalanes des de la perspectiva de gènere en els darrers trenta anys.

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The rate of food consumption is a major factor affecting success in scramble competition for a limited amount of easy-to-find food. Accordingly, several studies report positive genetic correlations between larval competitive ability and feeding rate in Drosophila; both become enhanced in populations evolving under larval crowding. Here, we report the experimental evolution of enhanced competitive ability in populations of D. melanogaster previously maintained for 84 generations at low density on an extremely poor larval food. In contrast to previous studies, greater competitive ability was not associated with the evolution of higher feeding rate; if anything, the correlation between the two traits across lines tended to be negative. Thus, enhanced competitive ability may be favored by nutritional stress even when competition is not intense, and competitive ability may be decoupled from the rate of food consumption.

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This work was conducted at the Universidade Estadual de Londrina (UEL), in Londrina, State of Paraná, Brazil, with the goal to study food-type soybean (Glycine max (L.) Merrill) genotypes performance for use in cultivation or crosses. A total of 104 genotypes were analyzed: 88 were food-type with large seeds, eight were food-type with small seeds, and eight-grain types adapted cultivars. The experimental plan was in randomized complete block design with four replications, and 12 traits of agronomic importance were considered. Genetic diversity was observed in the food-type germplasm. There were some genotypes with high yield adapted to a normal period of sowing. Soybean genetic improvement programs for direct human consumption in Brazil, either by means of Asiatic pure lines or by means of the incorporation of genes for late flowering in short-day conditions in this lines is highly viable.

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Plants such as Arabidopsis thaliana respond to foliar shade and neighbors who may become competitors for light resources by elongation growth to secure access to unfiltered sunlight. Challenges faced during this shade avoidance response (SAR) are different under a light-absorbing canopy and during neighbor detection where light remains abundant. In both situations, elongation growth depends on auxin and transcription factors of the phytochrome interacting factor (PIF) class. Using a computational modeling approach to study the SAR regulatory network, we identify and experimentally validate a previously unidentified role for long hypocotyl in far red 1, a negative regulator of the PIFs. Moreover, we find that during neighbor detection, growth is promoted primarily by the production of auxin. In contrast, in true shade, the system operates with less auxin but with an increased sensitivity to the hormonal signal. Our data suggest that this latter signal is less robust, which may reflect a cost-to-robustness tradeoff, a system trait long recognized by engineers and forming the basis of information theory.

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Light toxicity is suspected to enhance certain retinal degenerative processes such as age-related macular degeneration. Death of photoreceptors can be induced by their exposure to the visible light, and although cellular processes within photoreceptors have been characterized extensively, the role of the retinal pigment epithelium (RPE) in this model is less well understood. We demonstrate that exposition to intense light causes the immediate breakdown of the outer blood-retinal barrier (BRB). In a molecular level, we observed the slackening of adherens junctions tying up the RPE and massive leakage of albumin into the neural retina. Retinal pigment epithelial cells normally secrete vascular endothelial growth factor (VEGF) at their basolateral side; light damage in contrast leads to VEGF increase on the apical side - that is, in the neuroretina. Blocking VEGF, by means of lentiviral gene transfer to express an anti-VEGF antibody in RPE cells, inhibits outer BRB breakdown and retinal degeneration, as illustrated by functional, behavioral and morphometric analysis. Our data show that exposure to high levels of visible light induces hyperpermeability of the RPE, likely involving VEGF signaling. The resulting retinal edema contributes to irreversible damage to photoreceptors. These data suggest that anti-VEGF compounds are of therapeutic interest when the outer BRB is altered by retinal stresses.

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Tumour cells proliferate much faster than normal cells; nearly all anticancer treatments are toxic to both cell types, limiting their efficacy. The altered metabolism resulting from cellular transformation and cancer progression supports cellular proliferation and survival, but leaves cancer cells dependent on a continuous supply of energy and nutrients. Hence, many metabolic enzymes have become targets for new cancer therapies. In addition to its well-described roles in cell-cycle progression and cancer, the cyclin/CDK-pRB-E2F1 pathway contributes to lipid synthesis, glucose production, insulin secretion, and glycolytic metabolism, with strong effects on overall metabolism. Notably, these cell-cycle regulators trigger the adaptive "metabolic switch" that underlies proliferation.

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The purpose of the study was to evaluate the shear bond strength of stainless steel orthodontic brackets directly bonded to extracted human premolar teeth. Fifty teeth were randomly divided into ¿ve groups: (1) System One (chemically cured composite resin), (2) Light Bond (light-cured composite resin), (3) Vivaglass Cem (self-curing glass ionomer cement), (4) Fuji Ortho LC (light-cured glass ionomer cement) used after 37% orthophosphoric acid¿etching of enamel (5) Fuji Ortho LC without orthophosphoric acid¿etching. The brackets were placed on the buccal and lingual surfaces of each tooth, and the specimens were stored in distilled water (24 hours) at 378C and thermocycled. Teeth were mounted on acrylic block frames, and brackets were debonded using an Instron machine. Shear bond strength values at fracture (Nw)were recorded. ANOVA and Student-Newman-Keuls multiple comparison tests were performed (P , .05). Bonding failure site was recorded by stereomicroscope and analyzed by Chi-square test, selected specimens of each group were observed by scanning electron microscope. System One attained the highest bond strength. Light Bond and Fuji Ortho LC, when using an acid-etching technique, obtained bond strengths that were within the range of estimated bond strength values for successful clinical bonding. Fuji Ortho LC and Vivaglass Cem left an almost clean enamel surface after debracketing.

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About 30 million people live above 2500 m in the Andean Mountains of South America. Among them are 5.5 million Aymaras, an ethnic group with its own language, living on the altiplano of Bolivia, Peru, and northern Chile at altitudes of up to 4400 m. In this high altitude region traces of human population go back for more than 2000 years with constant evolutionary pressure on its residents for genetic adaptation to high altitude. Aymaras as the assumed direct descendents of the ancient cultures living in this region were the focus of much research interest during the last decades and several distinctive adaptation patterns to life at high altitude have been described in this ethnic group. The aim of this article was to review the physiology and pathophysiology of circulatory adaptation and maladaptation to longtime altitude exposure in Aymaras and Caucasians.

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Purpose: The retinal balance between pro- and anti-angiogenic factors is critical for angiogenesis control, but is also involved in cell survival. We previously reported upregulation of VEGF and photoreceptor (PR) cell death in the Light-damage (LD) model. Preliminary results showed that anti-VEGF can rescue PR from cell death. Thus, we investigated the role of VEGF on the retina and we herein described the effect of anti-VEGF antibody delivered by lentiviral gene transfer in this model.Methods: To characterize the action of VEGF during the LD, we exposed Balb/c mice subretinally injected with LV-anti-VEGF, or not, to 5'000 lux for 1h. We next evaluated the retinal function, PR survival and protein expression (VEGF, VEGFR1/2, Src, PEDF, p38MAPK, Akt, Peripherin, SWL-opsin) after LD. We analyzed Blood retinal barrier (BRB) integrity on flat-mounted RPE and cryosections stained with β-catenin, ZO-1, N-cadherin and albumin.Results: Results indicate that the VEGF pathway is modulated after LD. LD leads to extravascular albumin leakage and BRB breakdown: β-catenin, ZO-1 and N-cadherin translocate to the cytoplasm of RPE cells showing loss of cell cohesion. This phenomenon is in adequacy with the VEGF time-course expression. Assessment of the retinal function reveals that PR rescue correlates with the level of LV-anti-VEGF expression. Rhodopsin content was higher in the LV-anti-VEGF group than in controls and measures of the ONL thickness indicate that LV-anti-VEGF preserves by 82% the outer nuclear layer from degeneration. Outer segments (OS) appeared well organized with an appropriate length in the LV-anti-VEGF group compared to controls, and the expression of SWL-opsin is maintained in the OS without being mislocalized as in the LV-GFP group. Finally, LV-anti-VEGF treatment prevents BRB breakdown and maintained RPE cell integrity.Conclusions: This study involves VEGF in LD and highlights the prime importance of the BRB integrity for PR survival. Taken together, these results show that anti-VEGF is neuroprotective in this model and maintains functional PR layer in LD-treated mice.

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The adaptive function of melanin-based coloration is a long-standing debate. A recent genetic model suggested that pleiotropy could account for covariations between pigmentation, behaviour, morphology, physiology and life history traits. We explored whether the expression levels of genes belonging to the melanocortin system (MC1R, POMC, PC1/3, PC2 and the antagonist ASIP), which have many pleiotropic effects, are associated with melanogenesis (through variation in the expression of the genes MITF, SLC7A11, TYR, TYRP1) and in turn melanin-based coloration. We considered the tawny owl (Strix aluco) because individuals vary continuously from light to dark reddish, and thus, colour variation is likely to stem from differences in the levels of gene expression. We measured gene expression in feather bases collected in nestlings at the time of melanin production. As expected, the melanocortin system was associated with the expression of melanogenic genes and pigmentation. Offspring of darker reddish fathers expressed PC1/3 to lower levels but tended to express PC2 to higher levels. The convertase enzyme PC1/3 cleaves the POMC prohormone to obtain ACTH, while the convertase enzyme PC2 cleaves ACTH to produce α-melanin-stimulating hormone (α-MSH). ACTH regulates glucocorticoids, hormones that modulate stress responses, while α-MSH induces eumelanogenesis. We therefore conclude that the melanocortin system, through the convertase enzymes PC1/3 and PC2, may account for part of the interindividual variation in melanin-based coloration in nestling tawny owls. Pleiotropy may thus account for the covariation between phenotypic traits involved in social interactions (here pigmentation) and life history, morphology, behaviour and physiology.

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Unassembled immunoglobulin light chains expressed by the mouse plasmacytoma cell line NS1 (KNS1) are degraded in vivo with a half-life of 50-60 min in a way that closely resembles endoplasmic reticulum (ER)-associated degradation (Knittler et al., 1995). Here we show that the peptide aldehydes MG132 and PS1 and the specific proteasome inhibitor lactacystin effectively increased the half-life of KNS1, arguing for a proteasome-mediated degradation pathway. Subcellular fractionation and protease protection assays have indicated an ER localization of KNS1 upon proteasome inhibition. This was independently confirmed by the analysis of the folding state of KNS1and size fractionation experiments showing that the immunoglobulin light chain remained bound to the ER chaperone BiP when the activity of the proteasome was blocked. Moreover, kinetic studies performed in lactacystin-treated cells revealed a time-dependent increase in the physical stability of the BiP-KNS1complex, suggesting that additional proteins are present in the older complex. Together, our data support a model for ER-associated degradation in which both the release of a soluble nonglycosylated protein from BiP and its retrotranslocation out of the ER are tightly coupled with proteasome activity.

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The exchange of information during interactions of T cells with dendritic cells, B cells or other T cells regulates the course of T, B and DC-cell activation and their differentiation into effector cells. The tumor necrosis factor superfamily member LIGHT (homologous to lymphotoxin, exhibits inducible expression and competes with HSV glycoprotein D for binding to herpesvirus entry mediator, a receptor expressed on T lymphocytes) is transiently expressed upon T cell activation and modulates CD8 T cell-mediated alloreactive responses upon herpes virus entry mediator (HVEM) and lymphotoxin β receptor (LTβR) engagement. LIGHT-deficient mice, or WT mice treated with LIGHT-targeting decoy receptors HVEM-Ig, LTβR-Ig or sDcR3-Ig, exhibit prolonged graft survival compared to untreated controls, suggesting that LIGHT modulates the course and severity of graft rejection. Therefore, targeting the interaction of LIGHT with HVEM and/or LTβR using recombinant soluble decoy receptors or monoclonal antibodies represent an innovative therapeutic strategy for the prevention and treatment of allograft rejection and for the promotion of donor-specific tolerance.

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This article summarizes the basic principles of light microscopy, with examples of applications in biomedicine that illustrate the capabilities of thetechnique.